The effects of tanshinone IIA on hypoxia/reoxygenation-induced myocardial microvascular endothelial cell apoptosis in rats via the JAK2/STAT3 signaling pathway.
Abstract Source:Biomed Pharmacother. 2016年10月； 83：1116-1126。 EPUB 2016 8月20日。PMID： 275551758 27551758 Wei
Article Affiliation:Zhen-Tian Cui
Abstract:OBJECTIVE: This study aims to investigate the effects of tanshinone IIA on hypoxia/reoxygenation (H/R)-induced myocardial microvascular endothelial cell (MMEC) apoptosis in大鼠。
方法： mmecs隔离，培养和鉴定，将10天老化的大鼠分离，培养和鉴定，然后分为以下组：对照组，对照组，对照组，对照+tanshinone+tanshinone IIA（50μm）组，H/R Model Model Model Model Model Model Model Model Model h/R+Tans，R+TANS，R+TANSHON，R+TANSHON。E IIA（5μM）组，H/R+Tanshinone IIA（50μM）预处理组，H/R+AG490（50μM）预处理组和H/R+AG490（50μM）+Tanshinone IIA IIA IIA（50μM）预处理组。 MTT分析，TUNEL染色和流式细胞仪用于测量细胞活力和凋亡。 Western-blot were performed to detect protein expressions in JAK2/STAT3 signaling pathway.
RESULTS: Compared with control group, H/R group showed decreased cell viability, increased apoptosis rate, increased proportions of cells into G0/G1 phase, decreased proportions of cells in S phase and G2/M phase, as well作为JAK2，STAT3，P53，BAX，CASPASE-3，PJAK2和PSTAT3的上调表达式，以及BCl-2表达下调的表达（所有P <0.05）。与H/R组相比，H/R+Tanshinone IIA（5μM）组，H/R+Tanshinone IIA（50μm）组H/R+AG490（50μm）组和H/R+AG490（50μm）+Tanshinone IIA（50μm）组具有增加的细胞活力，减少了升华率将细胞的比例分为G0/G1相，S期和G2/M期的细胞比例升高，以及JAK2，STAT3，P53，P53，BAX，CASPASE-3，PJAK2，PJAK2和PSTAT3的下调表达，升高了Bcl-2的表达（所有P <0.05）。 The most remarkable changes were observed in H/R+AG490 (50μM)+tanshinone IIA (50μM) group.
CONCLUSION: Tanshinone IIA may attenuate H/R-induced MMEC apoptosis in rats by inhibiting the JAK2/STAT3 signaling pathway and调节p53，bax，caspase-3和bcl-2的表达，这可能会为MMEC提供Tanshinone IIA的保护作用。