Article(id=1291404931550933042, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1291404875351449891, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2025.09.009, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1735142400000, receivedDateStr=2024-12-26, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785824528825, onlineDateStr=2026-08-04, pubDate=1747411200000, pubDateStr=2025-05-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785824528825, onlineIssueDateStr=2026-08-04, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785824528825, creator=13701087609, updateTime=1785824528825, updator=13701087609, issue=Issue{id=1291404875351449891, tenantId=1146029695717560320, journalId=1246415772164075586, year='2025', volume='41', issue='9', pageStart='1201', pageEnd='1350', issueExtLink='null', onlineDate='null', pubDate='1747411200000', pubDateStr='2025-05-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785824515426, creator='13701087609', updateTime=1785824515426, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext=null, issueFiles=null, downloadFileDto=null}, startPage=1248, endPage=1253, ext={EN=ArticleExt(id=1291404931739676723, articleId=1291404931550933042, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Effects of pitavastatin on lipopolysaccharide-induced rat cardiomyocytes
via NLRP3 pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effects of pitavastatin on lipopolysaccharide (LPS)-induced H9c2 cells and its mechanism.
Methods H9c2 cells were divided into control group, model group (treated with 10 μg·mL-1 LPS), experimental group (after 1 μmol·L-1 pitavastatin treatment, 10 μg·mL-1 LPS treatment), and combination group [treated with 1.28 μmol·L-1 NLR family pyrin domain containing protein 3 (NLRP3) agonist on the basis of experimental group]. The NLRP3/cysteine-requiring aspartate protease 1 (caspase-1)/gasdermin D (GSDMD) signaling pathway related protein levels were detected by Western blot. The messenger ribonucleic acid (mRNA) relative expression levels related to inflammation and mitochondrial function were detected by quantitative real time polymerase chain reaction.
Results The relative expression levels of NLRP3 protein in control group, model group, experimental group and combination group were 1.00±0.15, 2.56±0.38, 1.35±0.19 and 2.15±0.31, respectively; the relative expression levels of caspase-1 protein were 1.00±0.18, 1.88±0.22, 1.22±0.20 and 1.75±0.22, respectively; the relative expression levels of GSDMD protein were 1.00±0.14, 2.12±0.32, 1.55±0.21 and 1.99±0.23, respectively; the relative expression levels of tumor necrosis factor-α mRNA were 1.00±0.15, 4.12±0.65, 2.11±0.29 and 3.54±0.48, respectively; the relative expression levels of interleukin-1β mRNA were 1.00±0.18, 3.33±0.39, 1.42±0.25 and 2.23±0.33, respectively; the relative expression levels of interleukin-18 mRNA were 1.00±0.14, 2.28±0.28, 1.33±0.26 and 1.98±0.22, respectively; the relative expression levels of PPAR-γ coactivator 1 alpha (PGC-1α) mRNA were 1.00±0.14, 0.45±0.07, 0.89±0.12 and 0.61±0.08, respectively; the relative expression levels of mitochondrial transcription factor A mRNA were 1.00±0.19, 0.53±0.07, 0.77±0.09 and 0.58±0.08, respectively; the relative expression levels of nuclear respiratory factor-1 mRNA were 1.00±0.17, 0.62±0.08, 0.85±0.13 and 0.65±0.08, respectively; the relative expression levels of uncoupling protein 2 mRNA were 1.00±0.15, 0.34±0.05, 0.92±0.16 and 0.48±0.07, respectively. The above indexes in model group were compared with those in control group, those in experimental group were compared with those in model group, and those in combination group were compared with those in experimental group, the differences were statistically significant (all P<0.05).
Conclusion Pitavastatin can inhibit inflammation, reduce pyroptosis of H9c2 cells, and protect mitochondrial function, which may be achieved by inhibiting the NLRP3/caspase-1/GSDMD signaling pathway.
, authors=Li LIN, Chun-ping LI, Bin LIU, Yuan-sheng SUN, Bao-cai FU, authorsList=Li LIN, Chun-ping LI, Bin LIU, Yuan-sheng SUN, Bao-cai FU, authorCompany=null, correspAuthors=Bao-cai FU, 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=1291404932167495732, articleId=1291404931550933042, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=匹伐他汀经NLRP3通路对脂多糖诱导大鼠心肌细胞的影响, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探讨匹伐他汀对脂多糖（LPS）诱导的H9c2细胞的影响及其机制。
方法 将H9c2细胞分为对照组（正常培养）、模型组（10 μg·mL-1 LPS处理）、实验组（1 μmol·L-1匹伐他汀处理后10 μg·mL-1 LPS处理）和联合组[在实验组基础之上，加入1.28 μmol·L-1NLR家族Pyrin域蛋白3（NLRP3）激动药]。用蛋白质印迹法检测NLRP3/半胱氨酸蛋白酶-1（caspase-1）/成孔蛋白（GSDMD）信号通路相关蛋白表达水平，用实时定量反转录聚合酶链反应检测炎症、线粒体功能相关信使核糖核酸（mRNA）相对表达水平。
结果 对照组、模型组、实验组和联合组的NLRP3蛋白相对表达水平分别为1.00±0.15、2.56±0.38、1.35±0.19和2.15±0.31，caspase-1蛋白相对表达水平分别为1.00±0.18、1.88±0.22、1.22±0.20和1.75±0.22，GSDMD蛋白相对表达水平分别为1.00±0.14、2.12±0.32、1.55±0.21和1.99±0.23，肿瘤坏死因子-α mRNA相对表达水平分别为1.00±0.15、4.12±0.65、2.11±0.29和3.54±0.48，白细胞介素-1β mRNA相对表达水平分别为1.00±0.18、3.33±0.39、1.42±0.25和2.23±0.33，白细胞介素-18 mRNA相对表达水平分别为1.00±0.14、2.28±0.28、1.33±0.26和1.98±0.22，PPARγ共激活因子-1α（PGC-1α）mRNA相对表达水平分别为1.00±0.14、0.45±0.07、0.89±0.12和0.61±0.08，线粒体转录因子A mRNA相对表达水平分别为1.00±0.19、0.53±0.07、0.77±0.09和0.58±0.08，核呼吸因子-1 mRNA相对表达水平分别为1.00±0.17、0.62±0.08、0.85±0.13和0.65±0.08，解耦联蛋白2 mRNA相对表达水平分别为1.00±0.15、0.34±0.05、0.92±0.16和0.48±0.07。模型组的上述指标与对照组相比，实验组的上述指标与模型组相比，联合组的上述指标与试验组相比，在统计学上差异均有统计学意义（均P<0.05）。
结论 匹伐他汀能够抑制炎症反应，减轻H9c2细胞焦亡，保护线粒体功能，这可能是通过抑制NLRP3/caspase-1/GSDMD信号通路实现的。
, authors=林丽, 李春平, 刘彬, 孙源胜, 付宝才, authorsList=林丽, 李春平, 刘彬, 孙源胜, 付宝才, authorCompany=null, correspAuthors=付宝才, authorNote=
林丽（1965-），女，主任医师，主要从事重症疾病方面的相关研究工作
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