首页> 外文期刊>Molecular medicine reports >Pachymic acid protects H9c2 cardiomyocytes from lipopolysaccharide-induced inflammation and apoptosis by inhibiting the extracellular signal-regulated kinase 1/2 and p38 pathways
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Pachymic acid protects H9c2 cardiomyocytes from lipopolysaccharide-induced inflammation and apoptosis by inhibiting the extracellular signal-regulated kinase 1/2 and p38 pathways

机译:通过抑制细胞外信号调节的激酶1/2和P38途径,通过脂多糖诱导的炎症和细胞凋亡来保护H9C2心肌细胞免受脂多糖诱导的炎症和细胞凋亡

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摘要

Pachymic acid (PA), a lanostane-type triterpenoid and the major component of Poria cocos alcoholic extracts, has various pharmacological effects, including anti-inflamma-tory, anti-oxidative and anti-apoptotic. However, few studies have investigated the effects of PA on lipopolysaccharide (LPS) -induced H9c2 cell apoptosis and inflammation, or identified the possible mechanisms underlying these effects. In the present study, H9c2 cardiomyocytes were stimulated by LPS and treated with or without PA. The increased mRNA expression levels of tumor necrosis factor-a, interleukin (IL)-1 and IL-6 induced by LPS were attenuated following treatment with PA. PA also attenuated LPS-induced apoptosis, as determined by a terminal deoxynucleotidyl transferase dUTP nick end labeling assay, and regulated the LPS-induced protein expression levels of caspase 3, 8 and 9. Furthermore, the phosphorylations of extracellular-regulated kinase (Erk) 1/2 and p38 in the LPS-treated H9c2 cells were inhibited by PA. These results suggested that treatment with PA prevented the LPS-induced inflammatory and apoptotic response in cardiomyocytes, which may be mediated by inhibition of the Erk1/2 and p38 pathways.
机译:嗜睡(PA),Lannostane型三萜类化合物和茯苓醇毒性提取物的主要成分,具有各种药理作用,包括抗炎药,抗氧化和抗凋亡。然而,很少有研究已经研究了PA对脂多糖(LPS)的影响 - 诱导的H9C2细胞凋亡和炎症,或确定了这些效果的可能机制。在本研究中,通过LPS刺激H9C2心肌细胞并用或没有PA处理。通过LPS诱导的肿瘤坏死因子-A,白细胞介素(IL)-1和IL-6的增加的MRNA表达水平衰减在用PA处理后衰减。 PA还通过末端脱氧核苷酸转移酶DUTP核心标记测定测定的LPS诱导的细胞凋亡,并调节了Caspase 3,8和9的LPS诱导的蛋白表达水平。此外,细胞外调节激酶(ERK)的磷酸化通过PA抑制LPS处理的H9C2细胞中的1/2和P38。这些结果表明,用PA治疗可通过抑制ERK1 / 2和P38途径介导的心肌细胞治疗LPS诱导的炎症和凋亡响应。

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