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Protective effect of tanshinone IIA on H2O2-induced oxidative stress injury in rat cardiomyocytes by activating Nrf2 pathway
Journal of Receptors and Signal Transduction ( IF 2.8 ) Pub Date : 2020-02-26 , DOI: 10.1080/10799893.2020.1731535
Guang Yang 1 , Fang Wang 2 , Yan Wang 3 , Xiaojing Yu 4 , Shaohui Yang 4 , Hongxia Xu 4 , Jiankun Xing 5
Affiliation  

Abstract To investigate the protective effect of tanshinone IIA on H2O2-induced oxidative stress injury in rat cardiomyocytes, and further to study its potential mechanisms. H9C2 cells were used to establish H2O2 injury model. The cell viability and apoptosis were detected by CCK-8 assay and flow cytometry, respectively. ELISA was used to detect the levels of lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px). Moreover, the levels of malondialdehyde (MDA) and catalase (CAT) were tested by TBA and visible light methods, respectively. The Nrf2 pathway-related proteins were detected by Western blot. To validate the protective effect of tanshinone IIA on rat cardiomyocytes is worked by regulating the Nrf2 pathway, we further silenced Nrf2 and the above experiments were repeated. Tanshinone IIA could promote the proliferation, and reduce the apoptosis and ROS of rat cardiomyocytes induced by H2O2. Tanshinone IIA also could increase the activity of SOD, CAT, and GSH-Px, and decreased the activity of MDA and LDH. The protein expression of Nrf2, HO-1, and NQO1 was significantly up-regulated in tanshinone IIA groups, while the protein expression of Keap1 was significantly down-regulated. A further study has shown that silenced Nrf2 has completely opposite results. All those results suggested that tanshinone IIA could protect H2O2-induced oxidative stress injury in rat cardiomyocytes by activating Nrf2 pathway.

中文翻译:

丹参酮ⅡA通过激活Nrf2通路对H2O2诱导的大鼠心肌细胞氧化应激损伤的保护作用

摘要 研究丹参酮IIA对H2O2诱导的大鼠心肌细胞氧化应激损伤的保护作用,并进一步研究其潜在机制。H9C2细胞用于建立H2O2损伤模型。分别通过CCK-8法和流式细胞术检测细胞活力和凋亡。ELISA用于检测乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的水平。此外,丙二醛(MDA)和过氧化氢酶(CAT)的水平分别通过TBA和可见光方法测试。通过蛋白质印迹检测 Nrf2 通路相关蛋白。为了验证丹参酮 IIA 对大鼠心肌细胞的保护作用是通过调节 Nrf2 途径起作用的,我们进一步沉默 Nrf2 并重复上述实验。丹参酮IIA可促进H2O2诱导的大鼠心肌细胞增殖,降低其凋亡和ROS。丹参酮IIA还可以增加SOD、CAT和GSH-Px的活性,降低MDA和LDH的活性。丹参酮IIA组Nrf2、HO-1和NQO1蛋白表达显着上调,而Keap1蛋白表达显着下调。进一步的研究表明,沉默的 Nrf2 具有完全相反的结果。所有这些结果表明丹参酮IIA可以通过激活Nrf2通路来保护H2O2诱导的大鼠心肌细胞氧化应激损伤。丹参酮IIA组Nrf2、HO-1和NQO1蛋白表达显着上调,而Keap1蛋白表达显着下调。进一步的研究表明,沉默的 Nrf2 具有完全相反的结果。所有这些结果表明丹参酮IIA可以通过激活Nrf2通路来保护H2O2诱导的大鼠心肌细胞氧化应激损伤。丹参酮IIA组Nrf2、HO-1和NQO1蛋白表达显着上调,而Keap1蛋白表达显着下调。进一步的研究表明,沉默的 Nrf2 具有完全相反的结果。所有这些结果表明丹参酮IIA可以通过激活Nrf2通路来保护H2O2诱导的大鼠心肌细胞氧化应激损伤。
更新日期:2020-02-26
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