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Effects of curcumin on the apoptosis of cardiomyocytes and the expression of NF-kappa B, PPAR-gamma and Bcl-2 in rats with myocardial infarction injury

机译:姜黄素对心肌梗死大鼠心肌细胞凋亡及NF-κB,PPAR-γ和Bcl-2表达的影响

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Curcumin is a natural polyphenol with powerful antioxidant and anti-inflammatory properties. The present study evaluated the protective effect of curcumin on myocardial injury in rats as well as the mechanisms underlying these effects, and examined the expression of nuclear factor-kappa B (NF-kappa B), peroxisome proliferator-activated receptor-gamma (PPAR-gamma) and B-cell leukemia/lymphoma-2 (Bcl-2) following myocardial infarction. A rat model of myocardial infarction was successfully established. Hematoxylin and eosin staining showed cellular atrophy and hyperchromatic cytoplasm in the myocardial infarction area. The myocardial cells displayed lysis and breakage of cardiac muscle fibers, karyopyknosis and karyorrhexis associated with infiltration of inflammatory cells and proliferation of fibrous tissue. Curcumin treatment at a dosage of 150 mg/kg/body weight resulted in an increase in surviving cells, fewer apoptotic cells, decreased proliferation of fibrous tissue and reduced infiltration of inflammatory cells, though necrosis was still present compared with the rats without curcumin treatment. The immunohistochemical assay demonstrated that curcumin treatment inhibited the expression of NF-kappa B, but increased the expression of PPAR-gamma. The results of the reverse transcription-polymerase chain reaction indicated that curcumin treatment significantly increased the mRNA expression levels of Bcl-2 (P<0.01). Therefore, curcumin antagonizes cardiomyocyte apoptosis and inhibits inflammatory cell infiltration following myocardial infarction, which may be associated with its inhibitory effects on the expression of NF-kappa B, and activating effects on the expression of PPAR-gamma and Bcl-2 in myocardial cells. Curcumin may be useful in clinical practice for saving more living heart muscle in the area of myocardial infarction and improving cardiac function following the elective opening of obstructed coronary arteries.
机译:姜黄素是一种天然的多酚,具有强大的抗氧化剂和抗炎特性。本研究评估了姜黄素对大鼠心肌损伤的保护作用及其潜在机制,并研究了核因子-κB(NF-κB),过氧化物酶体增殖物激活受体-γ(PPAR- γ)和心肌梗死后的B细胞白血病/淋巴瘤2(Bcl-2)。成功建立了大鼠心肌梗死模型。苏木精和曙红染色显示心肌梗死区细胞萎缩和细胞色素增高。心肌细胞显示出心肌纤维的溶解和断裂,核聚变和核溢漏,并伴有炎性细胞浸润和纤维组织增生。姜黄素的剂量为150 mg / kg /体重,导致存活细胞增加,凋亡细胞减少,纤维组织增殖减少,炎性细胞浸润减少,尽管与未进行姜黄素治疗的大鼠相比,坏死仍然存在。免疫组织化学分析表明姜黄素处理抑制了NF-κB的表达,但增加了PPAR-γ的表达。逆转录-聚合酶链反应的结果表明姜黄素处理显着提高了Bcl-2的mRNA表达水平(P <0.01)。因此,姜黄素拮抗心肌梗死后的心肌细胞凋亡并抑制炎性细胞浸润,这可能与其对NF-κB表达的抑制作用以及对心肌细胞中PPAR-γ和Bcl-2表达的活化作用有关。姜黄素在临床实践中可能有用,可在心肌梗塞区域节省更多的活心肌并在选择性开放梗阻性冠状动脉后改善心脏功能。

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