Salidroside Protects Against Hydrogen Peroxide-Induced Injury in Cardiac H9c2 Cells via PI3K-Akt Dependent Pathway
Salidroside Protects Against Hydrogen Peroxide-Induced Injury in Cardiac H9c2 Cells via PI3K-Akt Dependent Pathway
复制标题
红景天苷通过 PI3K-Akt 依赖性途径保护心脏 H9c2 细胞免受过氧化氢诱导的损伤
DOI：
10.1089/dna.2010.1183
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发表时间：
2011-10-01
影响因子：
3.1
通讯作者：
Jiang, Wei
中科院分区：
文献类型：
--
作者：
Zhu, Ye;Shi, Ya-Ping;Jiang, Wei
在心血管疾病中，氧化应激可导致严重的组织损伤。红景天苷具有很强的抗氧化和细胞保护作用，在开发心脏疾病氧化损伤的抗氧化疗法方面特别有兴趣。在过氧化氢(H_2O_2)诱导的氧化应激条件下，观察红景天苷对H9c2大鼠成肌细胞的药理作用。红景天苷以浓度依赖的方式减轻H_2O_2损伤的细胞活力，并有效抑制H_2O_2诱导的细胞丙二醛生成、致死性肌膜破坏、细胞坏死和细胞凋亡。在没有或存在H_2O_2刺激的情况下，红景天苷显著增强丝氨酸473位Akt的磷酸化；PI3K的特异性抑制剂Wortmannin取消了红景天苷的保护作用。红景天苷以PI3K依赖的方式增加细胞内过氧化氢酶和锰超氧化物歧化酶的mRNA表达和活性。结果表明，红景天苷通过激活PI3K/Akt通路，增加内源性PI3K依赖的抗氧化酶的表达和活性，从而保护心肌细胞免受氧化损伤。
Oxidative stress induces serious tissue injury in cardiovascular diseases. Salidroside, with its strong antioxidative and cytoprotective actions, is of particular interest in the development of antioxidative therapies for oxidative injury in cardiac diseases. We examined the pharmacological effects of salidroside on H9c2 rat cardiomyoblast cells under conditions of oxidative stress induced by hydrogen peroxide (H2O2) challenge. Salidroside attenuated H2O2-impaired cell viability in a concentration-dependent manner, and effectively inhibited cellular malondialdehyde production, lethal sarcolemmal disruption, cell necrosis, and apoptosis induced by H2O2 insult. Salidroside significantly augmented Akt phosphorylation at Serine 473 in the absence or presence of H2O2 stimulation; wortmannin, a specific inhibitor of PI3K, abrogated salidroside protection. Salidroside increased the intracellular mRNA expression and activities of catalase and Mn-superoxide dismutases in a PI3K-dependent manner. Our results indicated that salidroside protected cardiomyocytes against oxidative injury through activating the PI3K/Akt pathway and increasing the expression and activities of endogenous PI3K dependent antioxidant enzymes.