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Effects of aspirin on the apoptosis induced by hypoxia of human HTR-8/SVneo trophoblast cells, the expression of soluble fms-like tyrosine kinase receptor, and hypoxia-inducible factor-1αin the cells |
Xianning Central Hospital, The First Affilated Hospital of Hubei university of Scienc and Technology, 437000 |
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Abstract To explore the effects of aspirin on the apoptosis induced by hypoxia of human HTR-8/SVneo trophoblast cells, the expressions of soluble fms-like tyrosine kinase receptor-1 (sFlt), and hypoxia-inducible factor-1α(HIF-1α) in the cells. Methods: The human HTR-8/SVneo trophoblasts cells were divided into normal control group and hypoxia model group (the cells were given 2% O2, 5% CO2, and 93% N2). The cells in the two groups were treated by low-dose aspirin (0.05 mmol/L), medium-dose aspirin (0.1 mmol/L), or high-dose aspirin (0.2 mmol/L). After culture, MTT method was used to measure the cell viability, flow cytometry was used to measure cell apoptosis level and cell cycle, serum medium Matrigel culture was used to measure the cell angiogenesis ability, and the levels of sFlt-1 and HIF-1α in cells were detected by RT-PCR and Western blotting method. Results: The OD value, the survival rate, the angiogenesis ability, and the HIF-1α mRNA and protein expressions of the cells in the hypoxia model group were significantly lower than those of the cells in the normal control group, and which of the cells after treated by low aspirin, medium-dose, and high-dose of aspirin had decrease gradudally. The apoptosis rate, the G1 phase rate, and the sFlt-1 mRNA and protein expressions of the cells in the hypoxia model group were significantly higher than those of the cells in the normal control group, and which of the cells after treated by low aspirin, medium-dose, and high-dose of aspirin had increase gradudally (all P<0.05). Conclusion: The low dose of aspirin can promote the proliferation, angiogenesis, and inhibit apoptosis of HTR-8/SVneo cells under hypoxia. The mechanism is related to the low dose of aspirin inhibiting the expression of sFlt-1 and promoting the expression of HIF-1αof the HTR-8/SVneo cells under hypoxia.
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