张文强,文 亮,李 慧,叶飞林,薛 强.儿茶素经PI3K-Akt-eNOS信号通路对冠心病大鼠心肌损伤及抗炎作用分析[J].,2023,(9):1619-1623 |
儿茶素经PI3K-Akt-eNOS信号通路对冠心病大鼠心肌损伤及抗炎作用分析 |
Analysis of Myocardial Injury and Aanti-inflammatory Effect of Catechin in Coronary Heart Disease Rats through PI3K-Akt-eNOS Signaling Pathway |
投稿时间:2022-12-12 修订日期:2023-01-09 |
DOI:10.13241/j.cnki.pmb.2023.09.004 |
中文关键词: 儿茶素 PI3K-Akt-eNOS 冠心病 |
英文关键词: Catechin PI3K Akt - eNOS Coronary heart disease |
基金项目:国家自然科学基金青年项目(81600356) |
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中文摘要: |
摘要 目的:探讨儿茶素经PI3K-Akt-eNOS信号通路对冠心病大鼠心肌损伤及抗炎作用分析。方法:健康成年SPF级SD雄性大鼠,经腹腔注射垂体后叶素构建冠心病模型。采用Western blot法检测大鼠PI3K-Akt-eNOS信号通路相关蛋白的表达情况。采用ELISA法检测大鼠炎症因子和氧化应激指标的表达。观察并记录大鼠心肌损伤情况。结果:与空白组相比,模型组、儿茶素小剂量组、儿茶素中剂量组、儿茶素大剂量组的心肌缺血和心肌梗死面积均明显更高(P<0.05);儿茶素大剂量组心肌缺血和心肌梗死面积明显小于模型组、儿茶素小剂量组、儿茶素中剂量组(P<0.05);与空白组相比,模型组、儿茶素小剂量组、儿茶素中剂量组、儿茶素大剂量组的PI3K、p-Akt /Akt、p-eNOS /eNOS均明显更高(P<0.05);儿茶素大剂量组PI3K、p-Akt /Akt、p-eNOS /eNOS明显高于模型组、儿茶素小剂量组、儿茶素中剂量组(P<0.05);与空白组相比,模型组、儿茶素小剂量组、儿茶素中剂量组、儿茶素大剂量组的TNF-α、IL-1β、IL-18均明显更高(P<0.05);儿茶素大剂量组TNF-α、IL-1β、IL-18明显低于模型组、儿茶素小剂量组、儿茶素中剂量组(P<0.05);与空白组相比,模型组、儿茶素小剂量组、儿茶素中剂量组、儿茶素大剂量组的ROS、GSH-Px、MDA均明显更高(P<0.05);儿茶素大剂量组TNF-α、IL-1β、IL-18明显低于模型组、儿茶素小剂量组、儿茶素中剂量组(P<0.05)。结论:儿茶素可通过PI3K-Akt-eNOS信号通路靶向改善冠心病大鼠心肌炎症和氧化应激状况,进而发挥心肌保护作用。 |
英文摘要: |
ABSTRACT Objective: To investigate the effects of catechin on myocardial injury and anti-inflammatory effects in rats with coronary heart disease through PI3K-Akt-eNOS signaling pathway. Methods: Healthy adult SPF-grade SD male rats were injected with pituitrin intraperitoneally to establish coronary heart disease model. The expression of PI3K-Akt-eNOS signaling pathway was detected by Western blot. The expressions of inflammatory factors and oxidative stress were detected by ELISA. Myocardial injury in rats was observed and recorded. Results: Compared with blank group, myocardial ischemia and myocardial infarction area in model group, catechin low-dose group, catechin medium-dose group and catechin high-dose group were higher (P<0.05). The area of myocardial ischemia and myocardial infarction in catechin high-dose group was smaller than that in model group, catechin low-dose group and catechin medium-dose group (P<0.05). Compared with blank group, PI3K, p-Akt /Akt and P-ENOS /eNOS in model group, catechin low-dose group, catechin medium-dose group and catechin high-dose group were higher (P<0.05). PI3K, P-Akt /Akt and P-ENOS /eNOS in catechin high-dose group were higher than those in model group, catechin low-dose group and catechin medium-dose group (P<0.05); Compared with blank group, TNF-α, IL-1β and IL-18 in model group, catechin low-dose group, catechin medium-dose group and catechin high-dose group were higher (P<0.05). TNF-α, IL-1β and IL-18 in catechin high-dose group were lower than those in model group, catechin low-dose group and catechin medium-dose group (P<0.05). Compared with blank group, ROS, GSH-Px and MDA in model group, catechin low-dose group, catechin medium-dose group and catechin high-dose group were higher (P<0.05). TNF-α, IL-1β and IL-18 in catechin high-dose group were lower than those in model group, catechin low-dose group and catechin medium-dose group (P<0.05). Conclusion: Catechin can improve myocardial inflammation and oxidative stress in rats with coronary heart disease by targeting the PI3K-Akt-eNOS signaling pathway, and thus play a myocardial protective role. |
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