2022, Vol. 26 ›› Issue (30): 4852-4856

Mechanism underlying tanshinone IIA effect on survival and homing ability of myocardial precursor cells under hypoxia

Zhao Lin, Fan Chenxing, Li Kun   

Abstract: BACKGROUND: There are still many problems to be solved or perfected in the treatment of ischemic heart disease by stem cell transplantation. Among them, the key of stem cell transplantation in the treatment of ischemic heart disease is that the transplanted cells can home to the damaged myocardium and survive there.  
OBJECTIVE: To evaluate the effect of tanshinone IIA on the survival and homing ability of myocardial precursor cells under hypoxia and investigate its related mechanism.
METHODS: H9c2 cells were selected as the myocardial precursor cell model. The H9c2 cells were respectively intervened with cobalt chloride, tanshinone IIA+cobalt chloride and tanshinone IIA+cobalt chloride+AG126(ERK1/2 pathway inhibitor). Cell proliferation was detected with MTS method. Cell apoptosis was analyzed using flow cytometry. Cell migration was evaluated by scratch assay. The expression levels of ERK1/2 pathway related proteins (ERK1/2, p-ERK1/2, HIF-1α, cleaved caspase-3, and MMP-9) were assessed using western blot assay.  
RESULTS AND CONCLUSION: (1) Compared with the cobalt chloride group, the proliferation of H9c2 cells treated with cobalt chloride combined with tanshinone IIA was accelerated; the apoptosis was reduced; and the homing ability was enhanced. During this process, the expression of ERK1/2 had no significant changes (P > 0.05), but the expression levels of p-ERK1/2, HIF-1α, and MMP-9 were significantly increased (P < 0.05), and the expression of cleaved caspase-3 was significantly decreased (P < 0.05). (2) Compared with the cobalt chloride + tanshinone IIA group, the ERK1/2 pathway in H9c2 cells treated with cobalt chloride + tanshinone IIA + AG126 was significantly inhibited, and the ability of cell survival and migration to the injured area was significantly decreased. (3) The results showed that tanshinone IIA could promote the survival and homing ability of myocardial precursor cells under hypoxia by regulating ERK1/2 pathway.
Key words: ischemic heart disease, myocardial regeneration, tanshinone IIA, hypoxia, myocardial precursor cells, survival, homing, ERK1/2 pathway