黄芪注射液调节PI3K/ AKT 通路改善心肌梗死后心肌重塑
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(吉林大学基础医学院, 长春130021)

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R-33

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Protective effect of astragalus injection in cardiac remodeling after acute myocardial infarction via PI3K / AKT pathway activation
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(School of Basic Medical Sciences, Jilin University,Changchun 130021,China)

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    摘要:

    目的 探讨黄芪注射液(Astragalus injection, AS)对大鼠心肌梗死后心肌重塑的逆转作用及其作用机制?方法 通过结扎左冠状动脉前降支建立大鼠心肌梗死后心肌重塑模型,实验分为假手术组?模型组?AS 低剂量组(1 mL/ kg)及高剂量组(3 mL/ kg)?研究AS 治疗6 周对其生存百分率?血清中α 肌球蛋白重链(α-MHC)和大鼠N 端前脑钠素(NT-PROBNP)的影响;同时HE 染色及Masson 染色以检测心脏组织病理学变化及其心肌纤维化情况; ELISA 法检测各组血清中MDA?NO 及eNOS 的变化;Western blotting 法检测心肌细胞PI3K?P-AKT?及PeNOS蛋白的表达?结果 AS 高低剂量组与模型组比较,生存百分率有所提高,但无显著性差异;而AS 高剂量组α-MHC 及NT-PROBNP 较模型组显著降低( P < 0. 05); HE 及Masson 染色形态学检查显示,与模型组比较,AS 高剂量组炎细胞浸润?出血及纤维化程度减轻;高剂量组血清中MDA 降低( P < 0. 001)?NO 及eNOS 的升高( P <0. 05);Western blot 结果显示,AS 组的PI3K?p-AKT 表达量高于模型组( P <0. 05),p-eNOS 表达亦显著上升?结论 黄芪注射液可能通过激活PI3K/ AKT 通路降低氧化应激水平,从而抑制心肌梗死后心肌重塑?

    Abstract:

    Objective To examine the effect of Astragalus (AS) injection on post-myocardial infarction-inducedcardiac remodeling in rats, and explore potential mechanisms underlying such effects. Methods A cardiac remodelingpost-myocardial infarction model was prepared in rats, which were divided into four groups: sham operation, myocardialinfarction (model group), low-dose AS (ASL, 1 mL/ kg), and high-dose AS (ASH, 3 mL/ kg). Survival rate of the ratsand activities of the alpha isoform of myosin heavy chain (α-MHC) and N-terminal pro b-type natriuretic peptide (NTproBNP)in rat serum were measured after 6-week treatment. Histopathological changes and myocardial fibrosis wereobserved by light microscopy using hematoxylin and eosin, and Masson trichome staining. Quantification of malondialdehyde(MDA), nitric oxide ( NO), and endothelial nitric oxide synthase ( eNOS) were carried out using enzyme-linkedimmunosorbent assays. Protein expression of phosphatidylinositol 3 kinase (PI3K), phosphorylated AKT (p-AKT), and peNOSwere analyzed by western blotting. Results Compared with the model group, the survival rate of the ASL and ASHgroup were increased, but not significantly ( P > 0. 05). Meanwhile, α-MHC and NT-proBNP contents in the ASH groupwere reduced ( P < 0. 05). In addition, inflammation, hyperemia, and interstitial fibrosis were reduced in the ASH group.Moreover, the ASH group exhibited increased protein expression of PI3K and p-AKT in the injured heart ( P < 0. 05). peNOSexpression in the ASH group was increased compared with the model group ( P < 0. 05). Conclusions AS elicits anobvious protective effect on cardiac remodeling after myocardial infarction in rats. Activation of the PI3K/ AKT pathway mayactivate p-eNOS, which is involved in the mechanism by which AS prevents oxidative stress during cardiac remodeling.

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刘芬.黄芪注射液调节PI3K/ AKT 通路改善心肌梗死后心肌重塑[J].中国比较医学杂志,2019,29(6):32~38.

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  • 收稿日期:2018-10-10
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  • 在线发布日期: 2019-07-16
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