首页> 外文期刊>Molecular medicine reports >The protective effect of umbelliferone ameliorates myocardial injury following ischemia-reperfusion in the rat through suppression NLRP3 inflammasome and upregulating the PPAR-gamma
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The protective effect of umbelliferone ameliorates myocardial injury following ischemia-reperfusion in the rat through suppression NLRP3 inflammasome and upregulating the PPAR-gamma

机译:umbelliferone通过抑制NLRP3炎性缺血再灌注缺血再灌注并上调PPAR-Gamma后,Umbelliferone改善心肌损伤的保护作用

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The present study investigated whether the protective effect of umbelliferone could regulate myocardial injury following ischemia-reperfusion and improve mitochondrial respiratory function, thereby relieving myocardial injury following ischemia-reperfusion in rats. In the present study, the extent of inflammation and oxidative stress were analyzed using ELISA. Western blot analysis was employed to investigate the protein expression levels of the PYD domains-containing protein 3 (NLRP3) inflammasome and peroxisome proliferator-activated receptor-gamma (PPAR-gamma). Compared with the myocardial injury following ischemia-reperfusion group, umbelliferone significantly prevented myocardial injury, inhibited oxidative stress markers (superoxide dismutase and malondialdehyde), reduced inflammation (tumor necrosis factor-alpha and interleukin-6) and myocardial apoptosis levels (caspase-3/9 and apoptosis regular B-cell lymphoma-2-associated X protein) in the myocardial injury following ischemia-reperfusion group of rats. Umbelliferone treatment also suppressed NACHT, LRR and NLRP3 inflammasome activation and induced PPAR-gamma expression. The results of the present study suggested that the protective effect of umbelliferone may ameliorate myocardial injury following ischemia-reperfusion in the rat through the suppression of the NLRP3 inflammasome and upregulating PPAR-gamma expression.
机译:本实验研究伞形花内酯的保护作用是否能调节心肌损伤后缺血再灌注,改善线粒体呼吸功能,从而减轻对大鼠缺血再灌注心肌损伤。在本研究中,炎症和氧化应激的程度使用ELISA进行分析。用Western印迹分析,以研究含域-PYD蛋白3(NLRP3)炎性和过氧化物酶体增殖物激活受体-γ(PPAR-γ)的蛋白质表达水平。以下缺血再灌注组与心肌损伤相比,伞形酮显著防止心肌损伤,抑制氧化应激标记物(超氧化物歧化酶和丙二醛),减少炎症(肿瘤坏死因子α和白细胞介素-6)和心肌细胞凋亡的水平(胱天蛋白酶-3 / 9,并在心肌损伤以下缺血再灌注组大鼠凋亡定期B细胞淋巴瘤2相关的X蛋白)。伞形酮治疗也抑制NACHT,LRR和NLRP3炎性活化和诱导PPAR-γ的表达。本研究的结果表明,伞形酮的保护作用可以改善心肌损伤通过NLRP3炎性和上调PPAR-γ的表达的抑制以下在大鼠缺血再灌注。

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