Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry Original Paper Tanshinone Iia Improves Mir-133 Expression through Mapk Erk1/2 Pathway in Hypoxic Cardiac Myocytes Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry
Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry Original Paper Tanshinone Iia Improves Mir-133 Expression through Mapk Erk1/2 Pathway in Hypoxic Cardiac Myocytes Cellular Physiology and Biochemistry Cellular Physiology and Biochemistry
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通讯作者：
H. Shan;Li Zhang;Yanli Wu;Yumei Li;Chaoqian Xu;Xuelian Li;Daling Zhu;Yan Zhang;Shu Xing;Haoyan Wang;Zhihua Zhang
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作者：
H. Shan;Li Zhang;Yanli Wu;Yumei Li;Chaoqian Xu;Xuelian Li;Daling Zhu;Yan Zhang;Shu Xing;Haoyan Wang;Zhihua Zhang
丹参酮IIA是从中药丹参（Salvia miltiorrhiza）的根茎中提取的脂溶性抗炎活性化合物，丹参是用于治疗心血管疾病的著名传统中药。先前的研究已经确定丹参酮IIA抑制缺氧新生心肌细胞中miR-1的过表达。本研究旨在探讨丹参酮IIA对低氧条件下miR-133表达的影响。将新生大鼠心肌细胞置于37°C低氧环境（2%O2 + 93%N2 + 5%CO2）中培养24 h。采用MTT法、TUNEL法和流式细胞术（FCM）检测细胞凋亡。Western blot检测ERK 1/2的表达，Real-time PCR检测miR-133的表达。结果表明，缺氧可诱导细胞凋亡。TUNEL法检测可见典型的凋亡细胞，流式细胞仪检测缺氧组凋亡率为13.32%。丹参酮IIA可显著降低缺氧细胞的凋亡率。此外，缺氧细胞中miR-133的表达水平增加，丹参酮IIA进一步上调miR-133的表达。应激活化蛋白激酶MAPK ERK 1/2在缺氧条件下被激活，丹参酮IIA处理后进一步激活。本研究表明，丹参酮IIA通过激活MAPK ERK 1/2上调miR-133的表达，增强了新生心肌细胞对缺氧损伤的抵抗力。
Tanshinone IIA is a lipid-soluble pharmacologically active compound extracted from the rhizome of Chinese herb Salvia miltiorrhiza, a well-known traditional Chinese medicine used for the treatment of cardiovascular disorders. Previous studies have identified that tanshinone IIA inhibited overexpression of miR-1 in hypoxic neonatal cardiomyocytes. This study was designed to examine the effects of tanshinone IIA on miR-133 expression under hypoxic condition. Neonatal rat cardiomyocytes were cultured in a hypoxic environment (2% O 2 +93% N 2 +5% CO 2) at 37°C for 24 hours. MTT, TUNEL assays, and Flow Cytometry (FCM) were performed to identify cell apoptosis. Western blot was used to examine the expression of ERK1/2 and miR-133 level was quantified by Real-time PCR. Our results showed that apoptosis was induced by hypoxia. Typical apoptotic cells were seen by TUNEL assay, and FCM showed an apoptosis rate of 13.32% in hypoxic group. Apoptosis rate in hypoxic cells was reduced significantly by tanshinone IIA. In addition, the expression level of miR-133 was increased in hypoxic cells and further upregulated by tanshinone IIA. The stress-activated protein kinase MAPK ERK1/2 was activated by hypoxia and further increased with tanshinone IIA treatment. The present study demonstrated that tanshinone IIA enhanced cell resistance to hypoxic insult by upregulating miR-133 expression through activating MAPK ERK1/2 in neonatal cardiomyocytes.