Article(id=1322627838986007460, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1322627786464936095, articleNumber=null, orderNo=null, doi=null, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=1604246400000, acceptedDateStr=2020-11-02, onlineDate=1793268650051, onlineDateStr=2026-10-29, pubDate=1615737600000, pubDateStr=2021-03-15, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1793268650051, onlineIssueDateStr=2026-10-29, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1793268650051, creator=13701087609, updateTime=1793268650051, updator=13701087609, issue=Issue{id=1322627786464936095, tenantId=1146029695717560320, journalId=1235980733773295621, year='2021', volume='30', issue='5', pageStart='385', pageEnd='480', issueExtLink='null', onlineDate='null', pubDate='1615737600000', pubDateStr='2021-03-15', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1793268637529, creator='13701087609', updateTime=1793269201588, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1322630152530539005, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1322627786464936095, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1322630152530539006, tenantId=1146029695717560320, journalId=1235980733773295621, issueId=1322627786464936095, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=424, endPage=433, ext={EN=ArticleExt(id=1322627840768586661, articleId=1322627838986007460, tenantId=1146029695717560320, journalId=1235980733773295621, language=EN, title=The anti-diabetic chronic inflammation mechanism of berberine based on transcriptomics and proteomics analysis, columnId=null, journalTitle=Chinese Journal of New Drugs, columnName=null, runingTitle=null, highlight=null, articleAbstract=
Objective: LPS induces RAW264.7 cells to become an inflammation model, and uses transcriptomics and proteomics techniques to explore the anti-diabetic chronic inflammation mechanism of berberine.
Methods: After RAW264.7 cells induced by LPS (0.1 μg·mL-1) were incubated with berberine (1 μg·mL-1), protein and RNA were extracted, and proteomics and transcriptomics analysis were performed. Proteins and genes that were differentially expressed were found, and gene ontology (GO) enrichment analysis and Kyoto encyclopedia of genes and genomes (KEGG) pathway enrichment analysis were performed. STRING was used to draw interaction diagrams (PPI) to perform real-time fluorescence quantification of common differentially expressed proteins and genes PCR for verification.
Results: By comparing the model group with the berberine group, there are a total of 1 801 differentially expressed genes in transcriptomics, and 11 differentially expressed genes, such as Pdia4, Itgam, Hsp90b1, Prdx5, Pdia6, Myc, Fosl1, Il10, Ccl2, Lpin2 and Pik3r2, are related to inflammation. Proteomics obtained a total of 83 differentially expressed proteins, and 10 differentially expressed proteins were found, including Hsp90b1, Pdia6, Prdx5, Pdia4, Itgam, Stat1, Pgm2, Ptgs1, Nos2, Actb, are related to inflammation. There are 5 common differentially expressed proteins and genes.
Conclusion: Berberine may achieve anti-inflammatory effects by reducing the release of inflammatory factors, while reducing Hsp90b1, Pdia6, Prdx5, Pdia4, Itgam, PTGS1, NOS2 and IL-10, and increasing the production of Pik3r2 and LPIN 2 genes to further relieve abnormal metabolism and insulin resistance as well as reducing oxidative damage to the endoplasmic reticulum to treat diabetes.
, authors=Ying-qian CAO
1, Li-fen ZHOU
2, Hong YU
3, Ya-nan XUE
1, Zhi-fu AI
4, Xiao-quan LUO
4, Chang-hua ZHANG
1, authorsList=Ying-qian CAO, Li-fen ZHOU, Hong YU, Ya-nan XUE, Zhi-fu AI, Xiao-quan LUO, Chang-hua ZHANG, authorCompany=null, correspAuthors=Chang-hua ZHANG, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1322627841028633510, articleId=1322627838986007460, tenantId=1146029695717560320, journalId=1235980733773295621, language=CN, title=基于转录组学和蛋白质组学分析小檗碱抗糖尿病慢性炎症机制, columnId=1236330556003242277, journalTitle=中国新药杂志, columnName=实验研究, runingTitle=null, highlight=null, articleAbstract=
目的: 通过LPS诱导的RAW264.7细胞炎症模型,应用转录组学和蛋白质组学技术探究小檗碱抗糖尿病慢性炎症机制。
方法: RAW264.7细胞通过LPS(0.1 μg·mL-1)诱导,给予小檗碱(1 μg·mL-1),分别提取蛋白和RNA,进行蛋白质组学和转录组学分析,分别找出差异表达蛋白和差异表达基因,并进行基因本体(GO)富集分析和京都基因与基因组百科全书(KEGG)通路富集分析,并运用STRING进行绘制相互作用图(PPI),对共同差异表达蛋白和基因进行实时荧光定量PCR进行验证。
结果: 通过模型组与小檗碱组相比较,转录组学共有1 801个差异表达基因,找出11种差异表达基因Pdia4,Itgam,Hsp90b1,Prdx5,Pdia6,Myc,Fosl1,Il10,Ccl2,Lpin2,Pik3r2与炎症相关;蛋白质组学共得到83个差异表达蛋白,找出10个差异表达蛋白Hsp90b1,Pdia6,Prdx5,Pdia4,Itgam,Stat1,Pgm2,Ptgs1,Nos2,Actb与炎症相关;共同差异表达蛋白和基因共有5个。
结论: 小檗碱可能是通过减少炎症因子释放,同时减少Hsp90b1,Pdia6,Prdx5,Pdia4,Itgam,PTGS1,NOS2和IL-10及增加Pik3r2和LPIN 2基因的生成来达到抗炎作用,进一步缓解异常代谢和胰岛素抵抗以及减轻内质网氧化损伤来治疗糖尿病。
, authors=操映倩
1, 周立分
2, 余宏
3, 薛亚楠
1, 艾志福
4, 罗小泉
4, 章常华
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