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The effects of tanshinone IIA on hypoxia/reoxygenation-induced myocardial microvascular endothelial cell apoptosis in rats via the JAK2/STAT3 signaling pathway.
Biomedicine & Pharmacotherapy 2016 October
OBJECTIVE: This study aims to investigate the effects of tanshinone IIA on hypoxia/reoxygenation (H/R)-induced myocardial microvascular endothelial cell (MMEC) apoptosis in rats.
METHODS: MMECs from 10-days aged rats were isolated, cultured and identified, which were then divided into following groups: control group, control+tanshinone IIA (50μM) group, H/R model group, H/R+tanshinone IIA (5μM) group, H/R+tanshinone IIA (50μM) pre-treatment group, H/R+AG490 (50μM) pre-treatment group and H/R+AG490 (50μM)+tanshinone IIA (50μM) pre-treatment group. MTT assay, TUNEL staining and flow cytometry were used to measure the cellular viability and apoptosis. 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 as up-regulated expressions of JAK2, STAT3, p53, Bax, Caspase-3, pJAK2 and pSTAT3, and down-regulated Bcl-2 expression (all P<0.05). Compared with H/R group, H/R+tanshinone IIA (5μM) group, H/R+tanshinone IIA (50μM) group H/R+AG490 (50μM) group and H/R+AG490 (50μM)+tanshinone IIA (50μM) group had increased cell viability, decreased apoptosis rate, reduced proportions of cells into G0/G1 phase, elevated proportions of cells in S phase and G2/M phase, as well as down-regulated expressions of JAK2, STAT3, p53, Bax, Caspase-3, pJAK2 and pSTAT3, elevated expression of Bcl-2 (all 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 regulating the expressions of p53, Bax, Caspase-3 and Bcl-2, which may provide a protective effect of tanshinone IIA for MMECs.
METHODS: MMECs from 10-days aged rats were isolated, cultured and identified, which were then divided into following groups: control group, control+tanshinone IIA (50μM) group, H/R model group, H/R+tanshinone IIA (5μM) group, H/R+tanshinone IIA (50μM) pre-treatment group, H/R+AG490 (50μM) pre-treatment group and H/R+AG490 (50μM)+tanshinone IIA (50μM) pre-treatment group. MTT assay, TUNEL staining and flow cytometry were used to measure the cellular viability and apoptosis. 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 as up-regulated expressions of JAK2, STAT3, p53, Bax, Caspase-3, pJAK2 and pSTAT3, and down-regulated Bcl-2 expression (all P<0.05). Compared with H/R group, H/R+tanshinone IIA (5μM) group, H/R+tanshinone IIA (50μM) group H/R+AG490 (50μM) group and H/R+AG490 (50μM)+tanshinone IIA (50μM) group had increased cell viability, decreased apoptosis rate, reduced proportions of cells into G0/G1 phase, elevated proportions of cells in S phase and G2/M phase, as well as down-regulated expressions of JAK2, STAT3, p53, Bax, Caspase-3, pJAK2 and pSTAT3, elevated expression of Bcl-2 (all 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 regulating the expressions of p53, Bax, Caspase-3 and Bcl-2, which may provide a protective effect of tanshinone IIA for MMECs.
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