{"code":200,"data":{"content":[{"id":1877686621625786368,"dto":{"id":"38735402","regOrgCode":"00000","fullId":"PMID:38735402","cstrId":"cstr:00000.14.pmid.38735402","type":"PMID","index":"ids","data":{"id":"67720d04ab4f12186e16c8bb","cstrId":"cstr:00000.14.pmid.38735402","index":"pmid","type":"PMID","category":"14","ttl":180,"timeStamp":1735527684740,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/38735402"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736510350946},"ctime":1736510351004,"cost":58,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1877686919400398848,"dto":{"id":"38735402","regOrgCode":"00000","fullId":"PMID:38735402","cstrId":"cstr:00000.14.pmid.38735402","type":"PMID","index":"ids","data":{"id":"67720d04ab4f12186e16c8bb","cstrId":"cstr:00000.14.pmid.38735402","index":"pmid","type":"PMID","category":"14","snapshot":{"url":"https://pubmed.ncbi.nlm.nih.gov/38735402","htmlTitle":"A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation - PubMed","htmlPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-10/index.html","textPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-10/text.txt","snapshotImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-10/screenshot.png","fullPageImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-10/full_page_screenshot.png"},"ttl":180,"timeStamp":1735527684740,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/38735402"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; 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Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736511297919},"ctime":1736511297930,"cost":11,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1877690792873697280,"dto":{"id":"10.1186/s11658-022-00343-7","regOrgCode":"00000","fullId":"DOI:10.1186/s11658-022-00343-7","cstrId":"cstr:00000.14.doi.1186.s11658-022-00343-7","type":"DOI","index":"ids","data":{"id":"67722c5bab4f12186e16c8f7","cstrId":"cstr:00000.14.doi.1186.s11658-022-00343-7","index":"doi","type":"DOI","category":"14","snapshot":{"url":"https://dx.doi.org/10.1186/s11658-022-00343-7","htmlTitle":"Molecular mechanism of lncRNA SNHG12 in immune escape of non-small cell lung cancer through the HuR/PD-L1/USP8 axis | Cellular & Molecular Biology Letters | Full Text","htmlPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-08/index.html","textPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-08/text.txt","pdfLink":"https://cmbl.biomedcentral.com/counter/pdf/10.1186/s11658-022-00343-7.pdf","snapshotImgPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-08/screenshot.png","fullPageImgPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-08/full_page_screenshot.png","title":"Molecular mechanism of lncRNA SNHG12 in immune escape of non-small cell lung cancer through the HuR/PD-L1/USP8 axis","tags":["Fang Wei","Zeng Weiwei","Yang Zhenzhou","Zhang Jingyi","Xia Lei","Tan Benxu","Yu Xian","Huang Yusheng","Tan Xiangwu"],"absText":"<jats:title>Abstract</jats:title><jats:sec>\n                <jats:title>Background</jats:title>\n                <jats:p>The pivotal role of long noncoding RNAs (lncRNAs) in cancer immune responses has been well established. This study was conducted with the aim of exploring the molecular mechanism of lncRNA small nucleolar RNA host gene 12 (SNHG12) in immune escape of non-small cell lung cancer (NSCLC).</jats:p>\n              </jats:sec><jats:sec>\n                <jats:title>Methods</jats:title>\n                <jats:p>Expression of lncRNA SNHG12, programmed cell death receptor ligand 1 (PD-L1), ubiquitin-specific protease 8 (USP8), and human antigen R (HuR) in NSCLC tissues and cells was measured, and their binding relationship was determined. NSCLC cell proliferation and apoptosis were assessed. Peripheral blood mononuclear cells (PBMCs) were co-cultured with NSCLC cells. The ratio of CD8<jats:sup>+</jats:sup> T cells, PBMC proliferation, and inflammatory factors were determined. lncRNA SNHG12 localization was assessed via subcellular fractionation assay. The half-life period of mRNA was determined using actinomycin D. Xenograft tumor models were established to confirm the role of lncRNA SNHG12 in vivo.</jats:p>\n              </jats:sec><jats:sec>\n                <jats:title>Results</jats:title>\n                <jats:p>LncRNA SNHG12 was found to be prominently expressed in NSCLC tissues and cells, which was associated with a poor prognosis. Silencing lncRNA SNHG12 resulted in the reduction in proliferation and the promotion of apoptosis of NSCLC cells, while simultaneously increasing PBMC proliferation and the ratio of CD8<jats:sup>+</jats:sup> T cells. Mechanically, the binding of lncRNA SNHG12 to HuR improved mRNA stability and expression of PD-L1 and USP8, and USP8-mediated deubiquitination stabilized the protein level of PD-L1. Overexpression of USP8 or PD-L1 weakened the inhibition of silencing lncRNA SNHG12 on the immune escape of NSCLC. Silencing lncRNA SNHG12 restricted tumor growth and upregulated the ratio of CD8<jats:sup>+</jats:sup> T cells by decreasing USP8 and PD-L1.</jats:p>\n              </jats:sec><jats:sec>\n                <jats:title>Conclusion</jats:title>\n                <jats:p>LncRNA SNHG12 facilitated the immune escape of NSCLC by binding to HuR and increasing PD-L1 and USP8 levels.</jats:p>\n              </jats:sec>","year":2022},"ttl":180,"timeStamp":1735535707786,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://dx.doi.org/10.1186/s11658-022-00343-7","https://doi.org/10.1186/s11658-022-00343-7"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736511345480},"ctime":1736511345507,"cost":27,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1877691358488174592,"dto":{"id":"10.1186/s11658-022-00343-7","regOrgCode":"00000","fullId":"DOI:10.1186/s11658-022-00343-7","cstrId":"cstr:00000.14.doi.1186.s11658-022-00343-7","type":"DOI","index":"ids","data":{"id":"67722c5bab4f12186e16c8f7","cstrId":"cstr:00000.14.doi.1186.s11658-022-00343-7","index":"doi","type":"DOI","category":"14","snapshot":{"url":"https://dx.doi.org/10.1186/s11658-022-00343-7","htmlTitle":"Molecular mechanism of lncRNA SNHG12 in immune escape of non-small cell lung cancer through the HuR/PD-L1/USP8 axis | Cellular & Molecular Biology Letters | Full Text","htmlPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-08/index.html","textPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-08/text.txt","pdfLink":"https://cmbl.biomedcentral.com/counter/pdf/10.1186/s11658-022-00343-7.pdf","snapshotImgPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-08/screenshot.png","fullPageImgPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-08/full_page_screenshot.png","title":"Molecular mechanism of lncRNA SNHG12 in immune escape of non-small cell lung cancer through the HuR/PD-L1/USP8 axis","tags":["Fang Wei","Zeng Weiwei","Yang Zhenzhou","Zhang Jingyi","Xia Lei","Tan Benxu","Yu Xian","Huang Yusheng","Tan Xiangwu"],"absText":"<jats:title>Abstract</jats:title><jats:sec>\n                <jats:title>Background</jats:title>\n                <jats:p>The pivotal role of long noncoding RNAs (lncRNAs) in cancer immune responses has been well established. This study was conducted with the aim of exploring the molecular mechanism of lncRNA small nucleolar RNA host gene 12 (SNHG12) in immune escape of non-small cell lung cancer (NSCLC).</jats:p>\n              </jats:sec><jats:sec>\n                <jats:title>Methods</jats:title>\n                <jats:p>Expression of lncRNA SNHG12, programmed cell death receptor ligand 1 (PD-L1), ubiquitin-specific protease 8 (USP8), and human antigen R (HuR) in NSCLC tissues and cells was measured, and their binding relationship was determined. NSCLC cell proliferation and apoptosis were assessed. Peripheral blood mononuclear cells (PBMCs) were co-cultured with NSCLC cells. The ratio of CD8<jats:sup>+</jats:sup> T cells, PBMC proliferation, and inflammatory factors were determined. lncRNA SNHG12 localization was assessed via subcellular fractionation assay. The half-life period of mRNA was determined using actinomycin D. Xenograft tumor models were established to confirm the role of lncRNA SNHG12 in vivo.</jats:p>\n              </jats:sec><jats:sec>\n                <jats:title>Results</jats:title>\n                <jats:p>LncRNA SNHG12 was found to be prominently expressed in NSCLC tissues and cells, which was associated with a poor prognosis. Silencing lncRNA SNHG12 resulted in the reduction in proliferation and the promotion of apoptosis of NSCLC cells, while simultaneously increasing PBMC proliferation and the ratio of CD8<jats:sup>+</jats:sup> T cells. Mechanically, the binding of lncRNA SNHG12 to HuR improved mRNA stability and expression of PD-L1 and USP8, and USP8-mediated deubiquitination stabilized the protein level of PD-L1. Overexpression of USP8 or PD-L1 weakened the inhibition of silencing lncRNA SNHG12 on the immune escape of NSCLC. Silencing lncRNA SNHG12 restricted tumor growth and upregulated the ratio of CD8<jats:sup>+</jats:sup> T cells by decreasing USP8 and PD-L1.</jats:p>\n              </jats:sec><jats:sec>\n                <jats:title>Conclusion</jats:title>\n                <jats:p>LncRNA SNHG12 facilitated the immune escape of NSCLC by binding to HuR and increasing PD-L1 and USP8 levels.</jats:p>\n              </jats:sec>","year":2022},"ttl":180,"timeStamp":1735535707786,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://dx.doi.org/10.1186/s11658-022-00343-7","https://doi.org/10.1186/s11658-022-00343-7"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736511480332},"ctime":1736511480349,"cost":17,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1877692000782917632,"dto":{"id":"10.1186/s11658-022-00343-7","regOrgCode":"00000","fullId":"DOI:10.1186/s11658-022-00343-7","cstrId":"cstr:00000.14.doi.1186.s11658-022-00343-7","type":"DOI","index":"ids","data":{"id":"67722c5bab4f12186e16c8f7","cstrId":"cstr:00000.14.doi.1186.s11658-022-00343-7","index":"doi","type":"DOI","category":"14","snapshot":{"url":"https://dx.doi.org/10.1186/s11658-022-00343-7","htmlTitle":"Molecular mechanism of lncRNA SNHG12 in immune escape of non-small cell lung cancer through the HuR/PD-L1/USP8 axis | Cellular & Molecular Biology Letters | Full Text","htmlPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-10/index.html","textPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-10/text.txt","snapshotImgPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-10/screenshot.png","fullPageImgPath":"/ids/DOI/14/acf8e4ae0ff3705c89acf8f6730b2511/2025-01-10/full_page_screenshot.png"},"ttl":180,"timeStamp":1735535707786,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://dx.doi.org/10.1186/s11658-022-00343-7","https://doi.org/10.1186/s11658-022-00343-7"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736511633470},"ctime":1736511633479,"cost":9,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1877714055624531968,"dto":{"id":"37602300","regOrgCode":"00000","fullId":"PMID:37602300","cstrId":"cstr:00000.14.pmid.37602300","type":"PMID","index":"ids","data":{"id":"67722df6ab4f12186e16c8f9","cstrId":"cstr:00000.14.pmid.37602300","index":"pmid","type":"PMID","category":"14","snapshot":{"url":"https://pubmed.ncbi.nlm.nih.gov/37602300","htmlTitle":"lncRNA and circRNA expression profiles in the hippocampus of Aβ25‑35‑induced AD mice treated with Tripterygium glycoside - PubMed","htmlPath":"/ids/PMID/14/16d4e5b42e8eeedf54d3c6972a614b16/2025-01-10/index.html","textPath":"/ids/PMID/14/16d4e5b42e8eeedf54d3c6972a614b16/2025-01-10/text.txt","snapshotImgPath":"/ids/PMID/14/16d4e5b42e8eeedf54d3c6972a614b16/2025-01-10/screenshot.png","fullPageImgPath":"/ids/PMID/14/16d4e5b42e8eeedf54d3c6972a614b16/2025-01-10/full_page_screenshot.png","title":"lncRNA and circRNA expression profiles in the hippocampus of Aβ25‑35‑induced AD mice treated with Tripterygium glycoside","tags":["Ju Xiang","Liang Tang","Jianming Li","Dawei Yang","Yan Zhang","Yan Wang","Qin Xiang"],"absText":"Tripterygium glycosides (TG) have been reported to ameliorate Alzheimer's disease (AD), although the mechanism involved remains to be determined. In the present study, the lncRNA and circRNA expression profiles of an AD mouse model treated with TG were assessed using microarrays. lncRNAs, mRNAs, and circRNAs in the hippocampi of 3 AD+normal saline (NS) mice and 3 AD+TG mice were detected using microarrays. The most differentially expressed lncRNAs, mRNAs, and circRNAs were screened between the AD+NS and AD+TG groups. The differentially expressed lncRNAs and circRNAs were analyzed using GO enrichment and KEGG analyses. Co-expression analysis of lncRNAs, circRNAs, and mRNAs was performed by calculating the correlation coefficients. Protein-protein interaction (PPI) network analysis was performed on mRNAs using STRING. The lncRNA-target-transcription factor (TF) network was analyzed using the Network software. In total, 661 lncRNAs, 64 circRNAs, and 503 mRNAs were found to be differentially expressed in AD mice treated with TG. Pou4f1, Egr2, Mag, and Nr4a1 were the hub genes in the PPI network. The KEGG results showed that the mRNAs that were co-expressed with lncRNAs were enriched in the TNF, PI3K-Akt, and Wnt signaling pathways. LncRNA-target-TF network analysis indicated that TFs, including Cebpa, Zic2, and Rxra, were the most likely to regulate the detected lncRNAs. The circRNA-miRNA interaction network indicated that 275 miRNAs may bind to the 64 circRNAs. In conclusion, these findings provide a novel perspective on AD pathogenesis, and the detected lncRNAs, mRNAs, and circRNAs may serve as novel therapeutic targets for the management of AD.","year":2023},"ttl":180,"timeStamp":1735536118776,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/37602300"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736516891666},"ctime":1736516891793,"cost":127,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1877714178647662592,"dto":{"id":"38735402","regOrgCode":"00000","fullId":"PMID:38735402","cstrId":"cstr:00000.14.pmid.38735402","type":"PMID","index":"ids","data":{"id":"67720d04ab4f12186e16c8bb","cstrId":"cstr:00000.14.pmid.38735402","index":"pmid","type":"PMID","category":"14","snapshot":{"url":"https://pubmed.ncbi.nlm.nih.gov/38735402","htmlTitle":"A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation - PubMed","htmlPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-10/index.html","textPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-10/text.txt","snapshotImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-10/screenshot.png","fullPageImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-10/full_page_screenshot.png"},"ttl":180,"timeStamp":1735527684740,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/38735402"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736516921081},"ctime":1736516921098,"cost":17,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1877714223275057152,"dto":{"id":"38816229","regOrgCode":"00000","fullId":"PMID:38816229","cstrId":"cstr:00000.14.pmid.38816229","type":"PMID","index":"ids","data":{"id":"67722dfcab4f12186e16c8fb","cstrId":"cstr:00000.14.pmid.38816229","index":"pmid","type":"PMID","category":"14","snapshot":{"url":"https://pubmed.ncbi.nlm.nih.gov/38816229","htmlTitle":"Tauroursodeoxycholic Acid Reverses Dextran Sulfate Sodium-Induced Colitis in Mice via Modulation of Intestinal Barrier Dysfunction and Microbiome Dysregulation - PubMed","htmlPath":"/ids/PMID/14/aecb245d384c513b22c166f6909ab5a6/2025-01-08/index.html","textPath":"/ids/PMID/14/aecb245d384c513b22c166f6909ab5a6/2025-01-08/text.txt","snapshotImgPath":"/ids/PMID/14/aecb245d384c513b22c166f6909ab5a6/2025-01-08/screenshot.png","fullPageImgPath":"/ids/PMID/14/aecb245d384c513b22c166f6909ab5a6/2025-01-08/full_page_screenshot.png","title":"Tauroursodeoxycholic Acid Reverses Dextran Sulfate Sodium-Induced Colitis in Mice via Modulation of Intestinal Barrier Dysfunction and Microbiome Dysregulation","tags":["YinYue Xu","Menggai Zhang","Hua Luo","Longbiao Luo","Guangji Zhang","Sicen Wang","Yi Zhao","Xue Liu","Wanghui Jing","Sijing Dong","Hehe Shi"],"absText":"Ulcerative colitis (UC) is an immune-mediated inflammatory disease that can lead to persistent damage and even cancer without any intervention. Conventional treatments can alleviate UC symptoms but are costly and cause various side effects. Tauroursodeoxycholic acid (TUDCA), a secondary bile acid derivative, possesses anti-inflammatory and cytoprotective properties for various diseases, but its potential therapeutic benefits in UC have not been fully explored. Mice were subjected to colitis induction using 3% dextran sulfate sodium (DSS). The therapeutic effect of TUDCA was evaluated by body weight loss, disease activity index (DAI), colon length, and spleen weight ratio. Tissue pathology was assessed using H&E staining, while the levels of pro-inflammatory and anti-inflammatory cytokines in colonic tissue were quantified via ELISA. Tight junction proteins were detected by immunoblotting and intestinal permeability was assessed using fluorescein isothiocyanate (FITC)-dextran. Moreover, the gut microbiota was profiled using high-throughput sequencing of the 16S rDNA gene. TUDCA alleviated the colitis in mice, involving reduced DAI, attenuated colon and spleen enlargement, ameliorated histopathological lesions, and normalized levels of pro-inflammatory and anti-inflammatory cytokines. Furthermore, TUDCA treatment inhibited the downregulation of intestinal barrier proteins, including zonula occludens-1 and occludin, thus reducing intestinal permeability. The analysis of gut microbiota suggested that TUDCA modulated the dysbiosis in mice with colitis, especially for the remarkable rise in Akkermansia TUDCA exerted a therapeutic efficacy in DSS-induced colitis by reducing intestinal inflammation, protecting intestinal barrier integrity, and restoring gut microbiota balance. SIGNIFICANCE STATEMENT: This study demonstrates the potential therapeutic benefits of Tauroursodeoxycholic acid (TUDCA) in ulcerative colitis. TUDCA effectively alleviated colitis symptoms in mice, including reducing inflammation, restoring intestinal barrier integrity and the dysbiosis of gut microbiota. 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Conventional treatments can alleviate UC symptoms but are costly and cause various side effects. Tauroursodeoxycholic acid (TUDCA), a secondary bile acid derivative, possesses anti-inflammatory and cytoprotective properties for various diseases, but its potential therapeutic benefits in UC have not been fully explored. Mice were subjected to colitis induction using 3% dextran sulfate sodium (DSS). The therapeutic effect of TUDCA was evaluated by body weight loss, disease activity index (DAI), colon length, and spleen weight ratio. Tissue pathology was assessed using H&E staining, while the levels of pro-inflammatory and anti-inflammatory cytokines in colonic tissue were quantified via ELISA. Tight junction proteins were detected by immunoblotting and intestinal permeability was assessed using fluorescein isothiocyanate (FITC)-dextran. Moreover, the gut microbiota was profiled using high-throughput sequencing of the 16S rDNA gene. TUDCA alleviated the colitis in mice, involving reduced DAI, attenuated colon and spleen enlargement, ameliorated histopathological lesions, and normalized levels of pro-inflammatory and anti-inflammatory cytokines. Furthermore, TUDCA treatment inhibited the downregulation of intestinal barrier proteins, including zonula occludens-1 and occludin, thus reducing intestinal permeability. The analysis of gut microbiota suggested that TUDCA modulated the dysbiosis in mice with colitis, especially for the remarkable rise in Akkermansia TUDCA exerted a therapeutic efficacy in DSS-induced colitis by reducing intestinal inflammation, protecting intestinal barrier integrity, and restoring gut microbiota balance. SIGNIFICANCE STATEMENT: This study demonstrates the potential therapeutic benefits of Tauroursodeoxycholic acid (TUDCA) in ulcerative colitis. TUDCA effectively alleviated colitis symptoms in mice, including reducing inflammation, restoring intestinal barrier integrity and the dysbiosis of gut microbiota. This work highlights the promising role of TUDCA as a potentially alternative treatment, offering new insights into managing this debilitating condition.","year":2024},"ttl":180,"timeStamp":1735536124062,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/38816229"],"ip":"111.196.213.123","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/131.0.0.0 Safari/537.36","start":1736588105236},"ctime":1736588105248,"cost":12,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"111.196.213.123","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1878053447383785472,"dto":{"id":"38816229","regOrgCode":"00000","fullId":"PMID:38816229","cstrId":"cstr:00000.14.pmid.38816229","type":"PMID","index":"ids","data":{"id":"67722dfcab4f12186e16c8fb","cstrId":"cstr:00000.14.pmid.38816229","index":"pmid","type":"PMID","category":"14","snapshot":{"url":"https://pubmed.ncbi.nlm.nih.gov/38816229","htmlTitle":"Tauroursodeoxycholic Acid Reverses Dextran Sulfate Sodium-Induced Colitis in Mice via Modulation of Intestinal Barrier Dysfunction and Microbiome Dysregulation - PubMed","htmlPath":"/ids/PMID/14/aecb245d384c513b22c166f6909ab5a6/2025-01-11/index.html","textPath":"/ids/PMID/14/aecb245d384c513b22c166f6909ab5a6/2025-01-11/text.txt","snapshotImgPath":"/ids/PMID/14/aecb245d384c513b22c166f6909ab5a6/2025-01-11/screenshot.png","fullPageImgPath":"/ids/PMID/14/aecb245d384c513b22c166f6909ab5a6/2025-01-11/full_page_screenshot.png","title":"Tauroursodeoxycholic Acid Reverses Dextran Sulfate Sodium-Induced Colitis in Mice via Modulation of Intestinal Barrier Dysfunction and Microbiome Dysregulation","tags":["YinYue Xu","Menggai Zhang","Hua Luo","Longbiao Luo","Guangji Zhang","Sicen Wang","Yi Zhao","Xue Liu","Wanghui Jing","Sijing Dong","Hehe Shi"],"absText":"Ulcerative colitis (UC) is an immune-mediated inflammatory disease that can lead to persistent damage and even cancer without any intervention. Conventional treatments can alleviate UC symptoms but are costly and cause various side effects. Tauroursodeoxycholic acid (TUDCA), a secondary bile acid derivative, possesses anti-inflammatory and cytoprotective properties for various diseases, but its potential therapeutic benefits in UC have not been fully explored. Mice were subjected to colitis induction using 3% dextran sulfate sodium (DSS). The therapeutic effect of TUDCA was evaluated by body weight loss, disease activity index (DAI), colon length, and spleen weight ratio. Tissue pathology was assessed using H&E staining, while the levels of pro-inflammatory and anti-inflammatory cytokines in colonic tissue were quantified via ELISA. Tight junction proteins were detected by immunoblotting and intestinal permeability was assessed using fluorescein isothiocyanate (FITC)-dextran. Moreover, the gut microbiota was profiled using high-throughput sequencing of the 16S rDNA gene. TUDCA alleviated the colitis in mice, involving reduced DAI, attenuated colon and spleen enlargement, ameliorated histopathological lesions, and normalized levels of pro-inflammatory and anti-inflammatory cytokines. Furthermore, TUDCA treatment inhibited the downregulation of intestinal barrier proteins, including zonula occludens-1 and occludin, thus reducing intestinal permeability. The analysis of gut microbiota suggested that TUDCA modulated the dysbiosis in mice with colitis, especially for the remarkable rise in Akkermansia TUDCA exerted a therapeutic efficacy in DSS-induced colitis by reducing intestinal inflammation, protecting intestinal barrier integrity, and restoring gut microbiota balance. SIGNIFICANCE STATEMENT: This study demonstrates the potential therapeutic benefits of Tauroursodeoxycholic acid (TUDCA) in ulcerative colitis. TUDCA effectively alleviated colitis symptoms in mice, including reducing inflammation, restoring intestinal barrier integrity and the dysbiosis of gut microbiota. This work highlights the promising role of TUDCA as a potentially alternative treatment, offering new insights into managing this debilitating condition.","year":2024},"ttl":180,"timeStamp":1735536124062,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/38816229"],"ip":"111.196.213.123","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/131.0.0.0 Safari/537.36","start":1736597809055},"ctime":1736597809068,"cost":13,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"111.196.213.123","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1878627938128240640,"dto":{"id":"978-0-13-601970-1","regOrgCode":"00000","fullId":"ISBN:978-0-13-601970-1","cstrId":"cstr:00000.15.isbn.978-0-13-601970-1","type":"ISBN","index":"ids","data":{"id":"67721f47ab4f12186e16c8df","cstrId":"cstr:00000.15.isbn.978-0-13-601970-1","index":"isbn","type":"ISBN","category":"15","ttl":180,"timeStamp":1735532359565,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"15","url":["https://isbnsearch.org/isbn/978-0-13-601970-1"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; 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Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736738125654},"ctime":1736738125661,"cost":7,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1878642527586885632,"dto":{"id":"38735402","regOrgCode":"00000","fullId":"PMID:38735402","cstrId":"cstr:00000.14.pmid.38735402","type":"PMID","index":"ids","data":{"id":"67720d04ab4f12186e16c8bb","cstrId":"cstr:00000.14.pmid.38735402","index":"pmid","type":"PMID","category":"14","snapshot":{"url":"https://pubmed.ncbi.nlm.nih.gov/38735402","htmlTitle":"A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation - PubMed","htmlPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/index.html","textPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/text.txt","snapshotImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/screenshot.png","fullPageImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/full_page_screenshot.png","title":"A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation","tags":["Seema Saksena","Prabhdeep Kaur","Ravinder K Gill","Waddah A Alrefai","Anoop Kumar","Arvind Raj Vishnu Palani","Arivarasu N Anbazhagan","Sungmo Hong","Leeany Maletta","Shubha Priyamvada","Kimia Zadeh","Mansour Mohamadzadeh","Nazim Husain","Neelkanth Kulkarni","Shaunik Kapoor","Pradeep K Dudeja","Dulari Jayawardena","Yong Ge","Apurba Majumder","Yang-Ding Lin"],"absText":"Background & aims: Putative anion transporter-1 (PAT1, SLC26A6) plays a key role in intestinal oxalate and bicarbonate secretion. PAT1 knockout (PKO) mice exhibit hyperoxaluria and nephrolithiasis. Notably, diseases such as inflammatory bowel disease are also associated with higher risk of hyperoxaluria and nephrolithiasis. However, the potential role of PAT1 deficiency in gut-barrier integrity and susceptibility to colitis is currently elusive.\nMethods: Age-matched PKO and wild-type littermates were administered 3.5% dextran sulfate sodium in drinking water for 6 days. Ileum and colon of control and treated mice were harvested. Messenger RNA and protein expression of tight junction proteins were determined by reverse transcription polymerase chain reaction and western blotting. Severity of inflammation was assessed by measuring diarrheal phenotype, cytokine expression, and hematoxylin and eosin staining. Gut microbiome and associated metabolome were analyzed by 16S ribosomal RNA sequencing and mass spectrometry, respectively.\nResults: PKO mice exhibited significantly higher loss of body weight, gut permeability, colonic inflammation, and diarrhea in response to dextran sulfate sodium treatment. In addition, PKO mice showed microbial dysbiosis and significantly reduced levels of butyrate and butyrate-producing microbes compared with controls. Co-housing wild-type and PKO mice for 4 weeks resulted in PKO-like signatures on the expression of tight junction proteins in the colons of wild-type mice.\nConclusions: Our data demonstrate that loss of PAT1 disrupts gut microbiome and related metabolites, decreases gut-barrier integrity, and increases host susceptibility to intestinal inflammation. These findings, thus, highlight a novel role of the oxalate transporter PAT1 in promoting gut-barrier integrity, and its deficiency appears to contribute to the pathogenesis of inflammatory bowel diseases.","year":2024},"ttl":180,"timeStamp":1735527684740,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/38735402"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736738256720},"ctime":1736738256730,"cost":10,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1878690976273408000,"dto":{"id":"38735402","regOrgCode":"00000","fullId":"PMID:38735402","cstrId":"cstr:00000.14.pmid.38735402","type":"PMID","index":"ids","data":{"id":"67720d04ab4f12186e16c8bb","cstrId":"cstr:00000.14.pmid.38735402","index":"pmid","type":"PMID","category":"14","snapshot":{"url":"https://pubmed.ncbi.nlm.nih.gov/38735402","htmlTitle":"A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation - PubMed","htmlPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/index.html","textPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/text.txt","snapshotImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/screenshot.png","fullPageImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/full_page_screenshot.png","title":"A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation","tags":["Seema Saksena","Prabhdeep Kaur","Ravinder K Gill","Waddah A Alrefai","Anoop Kumar","Arvind Raj Vishnu Palani","Arivarasu N Anbazhagan","Sungmo Hong","Leeany Maletta","Shubha Priyamvada","Kimia Zadeh","Mansour Mohamadzadeh","Nazim Husain","Neelkanth Kulkarni","Shaunik Kapoor","Pradeep K Dudeja","Dulari Jayawardena","Yong Ge","Apurba Majumder","Yang-Ding Lin"],"absText":"Background & aims: Putative anion transporter-1 (PAT1, SLC26A6) plays a key role in intestinal oxalate and bicarbonate secretion. PAT1 knockout (PKO) mice exhibit hyperoxaluria and nephrolithiasis. Notably, diseases such as inflammatory bowel disease are also associated with higher risk of hyperoxaluria and nephrolithiasis. However, the potential role of PAT1 deficiency in gut-barrier integrity and susceptibility to colitis is currently elusive.\nMethods: Age-matched PKO and wild-type littermates were administered 3.5% dextran sulfate sodium in drinking water for 6 days. Ileum and colon of control and treated mice were harvested. Messenger RNA and protein expression of tight junction proteins were determined by reverse transcription polymerase chain reaction and western blotting. Severity of inflammation was assessed by measuring diarrheal phenotype, cytokine expression, and hematoxylin and eosin staining. Gut microbiome and associated metabolome were analyzed by 16S ribosomal RNA sequencing and mass spectrometry, respectively.\nResults: PKO mice exhibited significantly higher loss of body weight, gut permeability, colonic inflammation, and diarrhea in response to dextran sulfate sodium treatment. In addition, PKO mice showed microbial dysbiosis and significantly reduced levels of butyrate and butyrate-producing microbes compared with controls. Co-housing wild-type and PKO mice for 4 weeks resulted in PKO-like signatures on the expression of tight junction proteins in the colons of wild-type mice.\nConclusions: Our data demonstrate that loss of PAT1 disrupts gut microbiome and related metabolites, decreases gut-barrier integrity, and increases host susceptibility to intestinal inflammation. These findings, thus, highlight a novel role of the oxalate transporter PAT1 in promoting gut-barrier integrity, and its deficiency appears to contribute to the pathogenesis of inflammatory bowel diseases.","year":2024},"ttl":180,"timeStamp":1735527684740,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/38735402"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736749807786},"ctime":1736749807796,"cost":10,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395},{"id":1878691207174037504,"dto":{"id":"38735402","regOrgCode":"00000","fullId":"PMID:38735402","cstrId":"cstr:00000.14.pmid.38735402","type":"PMID","index":"ids","data":{"id":"67720d04ab4f12186e16c8bb","cstrId":"cstr:00000.14.pmid.38735402","index":"pmid","type":"PMID","category":"14","snapshot":{"url":"https://pubmed.ncbi.nlm.nih.gov/38735402","htmlTitle":"A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation - PubMed","htmlPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/index.html","textPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/text.txt","snapshotImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/screenshot.png","fullPageImgPath":"/ids/PMID/14/a40b8c68500bf48d5e202196d3a6b0e0/2025-01-13/full_page_screenshot.png","title":"A Direct Link Implicating Loss of SLC26A6 to Gut Microbial Dysbiosis, Compromised Barrier Integrity, and Inflammation","tags":["Seema Saksena","Prabhdeep Kaur","Ravinder K Gill","Waddah A Alrefai","Anoop Kumar","Arvind Raj Vishnu Palani","Arivarasu N Anbazhagan","Sungmo Hong","Leeany Maletta","Shubha Priyamvada","Kimia Zadeh","Mansour Mohamadzadeh","Nazim Husain","Neelkanth Kulkarni","Shaunik Kapoor","Pradeep K Dudeja","Dulari Jayawardena","Yong Ge","Apurba Majumder","Yang-Ding Lin"],"absText":"Background & aims: Putative anion transporter-1 (PAT1, SLC26A6) plays a key role in intestinal oxalate and bicarbonate secretion. PAT1 knockout (PKO) mice exhibit hyperoxaluria and nephrolithiasis. Notably, diseases such as inflammatory bowel disease are also associated with higher risk of hyperoxaluria and nephrolithiasis. However, the potential role of PAT1 deficiency in gut-barrier integrity and susceptibility to colitis is currently elusive.\nMethods: Age-matched PKO and wild-type littermates were administered 3.5% dextran sulfate sodium in drinking water for 6 days. Ileum and colon of control and treated mice were harvested. Messenger RNA and protein expression of tight junction proteins were determined by reverse transcription polymerase chain reaction and western blotting. Severity of inflammation was assessed by measuring diarrheal phenotype, cytokine expression, and hematoxylin and eosin staining. Gut microbiome and associated metabolome were analyzed by 16S ribosomal RNA sequencing and mass spectrometry, respectively.\nResults: PKO mice exhibited significantly higher loss of body weight, gut permeability, colonic inflammation, and diarrhea in response to dextran sulfate sodium treatment. In addition, PKO mice showed microbial dysbiosis and significantly reduced levels of butyrate and butyrate-producing microbes compared with controls. Co-housing wild-type and PKO mice for 4 weeks resulted in PKO-like signatures on the expression of tight junction proteins in the colons of wild-type mice.\nConclusions: Our data demonstrate that loss of PAT1 disrupts gut microbiome and related metabolites, decreases gut-barrier integrity, and increases host susceptibility to intestinal inflammation. These findings, thus, highlight a novel role of the oxalate transporter PAT1 in promoting gut-barrier integrity, and its deficiency appears to contribute to the pathogenesis of inflammatory bowel diseases.","year":2024},"ttl":180,"timeStamp":1735527684740,"permission":{"write":"SM2:MFkwEwYHKoZIzj0CAQYIKoEcz1UBgi0DQgAE1b4Zx33RU4klVm9MEHSX8ZawU0/t/g/UTbJeJKbneJajOiozE5HRSsLblY0JJy665PsAlIxLGOyRt9hKVNq1KA=="}},"category":"14","url":["https://pubmed.ncbi.nlm.nih.gov/38735402"],"ip":"124.127.236.95","useragent":"Mozilla/5.0 (Windows NT 10.0; Win64; x64) AppleWebKit/537.36 (KHTML, like Gecko) Chrome/130.0.0.0 Safari/537.36","start":1736749862838},"ctime":1736749862849,"cost":11,"brand":"Windows","os":"Windows 10 or Windows Server 2016","browser":"Chrome","ip":"124.127.236.95","country":"中国","province":"北京市","city":"北京","lat":39.911,"lng":116.395}],"pageable":{"sort":{"sorted":false,"unsorted":true,"empty":true},"offset":0,"pageNumber":0,"pageSize":20,"paged":true,"unpaged":false},"last":false,"totalPages":76,"totalElements":1518,"size":20,"number":0,"sort":{"sorted":false,"unsorted":true,"empty":true},"first":true,"numberOfElements":20,"empty":false}}