石斛碱通过调节自噬对心肌梗死大鼠心功能障碍的影响

IF 0.1 4区 医学
Juan Fan, Yi Zhang
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引用次数: 0

摘要

目的:观察石斛碱对大鼠心肌梗死后心功能不全的影响及其作用机制。材料:将27只大鼠分为假手术组、模型组和Den组,给药2周的大鼠用超声检测其心功能和结构;HE和Masson染色观察其心肌病理变化,TUNEL染色观察其凋亡细胞数;ELISA法检测其血清LDH和CK-MB活性;WB和免疫组织化学检测心肌自噬蛋白的表达。结果:模型组心功能下降,心肌纤维化面积增大,血清LDH和CK-MB活性增加,心肌组织结构损伤和凋亡细胞数增加,LAMP2表达下调,Beclin1、LC3-II/LC3-I和P62表达上调。对于心肌梗死大鼠,Den改善了心功能,减少了心肌纤维化面积,降低了血清LDH和CK-MB的活性,减轻了心肌结构的损伤,降低了心肌组织中的凋亡细胞数量,上调了Beclin1、LAMP2和LC3-II的表达,下调P62以促进心肌梗死损伤心肌的自噬。结论:Den通过Beclin1/LAMP2途径改善自噬体的形成和自噬流量,从而减轻心肌梗死后的心功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of Dendrobine on Cardiac Dysfunction in Rats with Myocardial Infarction by Regulating Autophagy
Aim: To observe Dendrobine (Den) on rats with post-myocardial infarction cardiac dysfunction and mechanism. Materials: Dividing 27 rats as Sham, Model and Den groups, rats treated with two weeks of drug had their cardiac function and structure measured by ultrasound; their myocardial pathological changes observed by HE and Masson staining and observe apoptosis cell number by TUNEL staining; their serum activities of LDH and CK-MB detected by ELISA; myocardial autophagy protein expressions detected by WB and immunohistochemistry. Results: Model group displayed decreased cardiac function levels, enlarged area of myocardial fibrosis, more serum activities of LDH and CK-MB, increased myocardial tissue structural damage and apoptosis cell number, downregulated LAMP2 expression, and up-regulated expressions of Beclin1, LC3-II/LC3-I rate, and P62. To rat victims of myocardial infarction, Den improved cardiac function, reduced area of myocardial fibrosis, compromised activities of serum LDH and CK-MB, and relieved damage in myocardial structure, decreased apoptosis cell number in myocardial tissue, up-regulated the expressions of Beclin1, LAMP2 and LC3-II, and down-regulated P62 to promote the autophagy in myocardium damaged by myocardial infarction. Conclusion: Den alleviates post-myocardial infarction cardiac dysfunction through improvement of autophagosomes formation and autophagic flux via Beclin1/LAMP2 pathway.
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