Protective effects of tanshinone IIA on myocardial ischemia reperfusion injury by reducing oxidative stress, HMGB1 expression, and inflammatory reaction
Protective effects of tanshinone IIA on myocardial ischemia reperfusion injury by reducing oxidative stress, HMGB1 expression, and inflammatory reaction
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DOI：
10.3109/13880209.2015.1005753
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发表时间：
2015-01-01
影响因子：
3.8
通讯作者：
Tang, Guanmin
中科院分区：
文献类型：
--
作者：
Hu, Huilin;Zhai, Changlin;Tang, Guanmin
背景：丹参酮IIA(TSA)对大鼠心肌缺血的保护作用已有报道，但其作用机制尚未完全阐明。目的：进一步验证TSA对大鼠心肌缺血再灌注损伤的保护作用，并阐明其可能的机制。材料与方法：大鼠每日腹腔注射丹参酮(TSA)10、20、40 mg/kgbw，连续15d，结扎冠状动脉前降支30min，再灌流120min，建立大鼠心肌缺血再灌注模型。结果：与IR组比较，L-TSA组、M-TSA组和H-TSA组心肌梗死面积百分比分别减少1.2 1%、4.2 6%和12.5 0%，CK活性分别降低7.4%、11.2%和12.5%，AST活性降低(p5 0.0 5)。与IR组比较，L-TSA组、M-TSA组、H-TSA组超氧化物歧化酶、谷胱甘肽过氧化物酶活性升高，丙二醛、肿瘤坏死因子-α、IL-6、诱导型一氧化氮合酶水平降低(p50.05)。同时，与IR组比较，L-TSA组、M-TSA组和H-TSA组HMGB1表达分别降低21.9%、32.4%和35.6%。讨论与结论：TSA对心肌缺血再灌注损伤的保护作用可能是通过抑制再灌注引起的ROS升高来实现的，从而减轻HMGB1的表达，抑制炎症反应。
Context: Although there were reports on the protective functions of tanshinone IIA (TSA) on rat myocardial ischemia, the exerting mechanism has not been completely clarified.Objective: An attempt was made to further verify the protective effect of TSA on myocardial ischemia reperfusion injury and elucidate its underlying mechanism.Materials and methods: The rats were given TSA (10, 20, and 40 mg/kg bw per day) in intraperitoneal injection for 15 d. Rami anterior descending branch of coronary artery was ligated for 30 min and then re-perfused for 120 min to establish a reperfusion model. Effects of TSA on the infarct area, creatine kinase (CK), aspartate aminotransferase (AST), high mobility group box B1 protein (HMGB1), and inflammation and oxidation were investigated.Results: Compared with those in the IR group, infarct size percentages of rats' myocardium in L-TSA, M-TSA, and H-TSA groups were reduced by 1.21, 4.26, and 12.50%, respectively, CK activities by 7.4, 11.2, and 12.5%, respectively, and AST activities also declined (p50.05). Furthermore, compared with those in the IR group, SOD and GSH-Px activities increased, and MDA, TNF-alpha, IL-6, and iNOS levels decreased in L-TSA, M-TSA, and H-TSA groups (p50.05). Meanwhile, compared with those in the IR group, HMGB1 expressions in L-TSA, M-TSA, and H-TSA groups were lowered by 21.9, 32.4, and 35.6%, respectively.Discussion and conclusion: The protective function of TSA on myocardial ischemia reperfusion injury may be possibly exerted by inhibiting the increase of ROS caused by the reperfusion to attenuate the expression of HMGB1 and inhibit inflammation.