首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Effective Components of Panax quinquefolius and Corydalis tuber Protect Myocardium through Attenuating Oxidative Stress and Endoplasmic Reticulum Stress
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Effective Components of Panax quinquefolius and Corydalis tuber Protect Myocardium through Attenuating Oxidative Stress and Endoplasmic Reticulum Stress

机译:西洋参和延胡索的有效成分通过减轻氧化应激和内质网应激保护心肌

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摘要

Both oxidative stress and endoplasmic reticulum stress (ERS) have been implicated in carcinogenesis and neurological diseases, while there are few reports about the mechanisms of them in the progression of acute myocardial infarction (AMI). This study examined oxidative stress and ERS in a rat model of AMI and evaluated their role in therapy by metoprolol and effective components of Panax quinquefolius and Corydalis tuber (EPC). In the present study a rat model of AMI was established by ligation of the left anterior descending coronary artery. After oral administration of metoprolol or low-to-high doses of EPC for 2 weeks, serum malondialdehyde (MDA), superoxide dismutase (SOD), and 8-iso-prostaglandin F2α (8-iso-PGF2α) were detected using enzyme-linked immunosorbent assay (ELISA). Quantitative real-time PCR and Western blotting were used to examine mRNA and protein expressions of the hallmarks of ERS-glucose-regulated protein-78 (GRP78) and CCAAT/enhancer-binding protein homologous protein (CHOP). We confirmed that both metoprolol and moderate-to-high dose of EPC decreased 8-iso-PGF2α serum level and downregulated the mRNA and protein expressions of GRP78 and CHOP in myocardium, while EPC also increased SOD serum level. These results indicated that metoprolol and EPC protect the myocardium by attenuating oxidative stress and ERS induced by myocardial infarction, highlighting the ERS pathways as potential therapeutic targets for AMI.
机译:氧化应激和内质网应激(ERS)都与致癌和神经系统疾病有关,而关于它们在急性心肌梗死(AMI)进程中的机制的报道很少。这项研究检查了AMI大鼠模型中的氧化应激和ERS,并评估了它们在美托洛尔以及西洋参和延胡索(EPC)的有效成分治疗中的作用。在本研究中,通过结扎左冠状动脉前降支建立了AMI大鼠模型。口服美托洛尔或低至高剂量的EPC 2周后,使用酶联法检测了血清丙二醛(MDA),超氧化物歧化酶(SOD)和8-异前列腺素F2α(8-异-PGF2α)免疫吸附测定(ELISA)。实时定量PCR和Western印迹用于检查ERS葡萄糖调节蛋白78(GRP78)和CCAAT /增强子结合蛋白同源蛋白(CHOP)标志的mRNA和蛋白表达。我们证实美托洛尔和中至高剂量的EPC均可降低心肌中的8-iso-PGF2α血清水平,并下调心肌GRP78和CHOP的mRNA和蛋白表达,而EPC还可提高SOD血清水平。这些结果表明,美托洛尔和EPC通过减轻心肌梗死诱导的氧化应激和ERS保护心肌,突出了ERS途径作为AMI的潜在治疗靶点。

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