狼疮通过调节NF-(公式:见正文)B和Nrf2通路减轻大鼠心肌缺血再灌注损伤。

Jing Li, Xuming Ma, Jun Yang, Lu Wang, Yan Huang, Yan Zhu
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引用次数: 1

摘要

心血管疾病是一个全球性的健康问题。先前的研究表明,它涉及急性心肌梗死和缺血再灌注(I/R)损伤。心肌I/R损伤机制复杂。但认识其机制将带来重要的临床意义。木犀草素广泛存在于中草药中,并已被证明具有多种生物活性。然而,羽扇豆醇在心肌缺血再灌注损伤(MIRI)过程中的药理作用尚不清楚。本研究采用大鼠心肌I/R模型,用2,3,5-三苯基氯化四氮唑(TTC)染色法测定心肌的形态学变化。通过实时定量PCR(qRT-PCR)和ELISA评估IL-10、IL-1[公式:见正文]、TNF-[公式:见正文]和IL-6的表达水平。酶联免疫吸附法测定肌酸激酶MB同工酶(CK-MB)、乳酸脱氢酶(LDH)和炎性细胞因子的表达水平。TUNEL染色测定细胞凋亡率。研究结果表明,羽扇豆醇显著减少I/R后的心肌梗死,并改善I/R诱导的心肌炎症、细胞凋亡和氧化应激。此外,我们的研究结果表明,羽扇豆醇通过调节NF-[公式:见正文]B和Nrf2信号通路,对MIRI诱导的心肌梗死具有保护作用。总之,本研究首次阐明了羽扇豆醇对I/R诱导的大鼠心肌梗死的心脏保护作用,这可能是由于其抗氧化、抗炎和抗凋亡活性。我们的研究还强调了NF-[公式:见正文]B和Nrf2信号传导的机制,通过该机制,羽扇豆醇可能是一种很有前途的预防I/R诱导的心肌梗死的药物。
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Lupeol Alleviates Myocardial Ischemia-Reperfusion Injury in Rats by Regulating NF-[Formula: see text]B and Nrf2 Pathways.
Cardiovascular disease is a global health problem. Previous studies revealed that it involves acute myocardial infarction and ischemia-reperfusion (I/R) injury. The mechanism of myocardial I/R injury is complex. But recognizing its mechanisms will bring important clinical significance. Lupeol is widely found in Chinese medicinal herbs and has been shown to have a variety of bio-activities. However, the pharmacological action of lupeol in the progress of myocardial ischemia-reperfusion injury (MIRI) is unclear. This study used a rat myocardial I/R model and the morphological changes in myocardium were determined by 2,3,5-triphenyltetrazolium chloride (TTC) staining. The expression levels of IL-10, IL-1[Formula: see text], TNF-[Formula: see text], and IL-6 were assessed by quantitative real-time PCR (qRT-PCR) and ELISA. The expression levels of MB isoenzyme of creatine kinase (CK-MB), lactate dehydrogenase (LDH) level and inflammatory cytokines were quantified using ELISA. The cellular apoptotic rate was determined by TUNEL staining. The findings showed that lupeol significantly decreased myocardial infarction after I/R and ameliorated I/R-induced myocardial inflammation, apoptosis, and oxidative stress. Furthermore, our results suggested that lupeol protected against MIRI-induced myocardial infarction through modulation of NF-[Formula: see text]B and Nrf2 signaling pathways. In summary, this study first clarified the cardioprotective effects of lupeol against I/R-induced myocardial infarction in rats, which could be due to its anti-oxidant, anti-inflammatory, and anti-apoptotic activities. Our study also highlighted a mechanism of NF-[Formula: see text]B and Nrf2 signaling, through which lupeol could be a promising agent in protecting against I/R-induced myocardial infarction.
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