The Effects Of Simvastatin On The Apoptosis Of Human Pulmonary Microvascular Endothelial Cell Induced By Neurogenic Pulmonary Edema Rats Serum

Objective: To investigate the effects of simvastatin on the apoptosis of Human Pulmonary microvascular endothelial cell induced by neurogenic pulmonary edema rats serum and its mechanism.Methods: 50 healthy male SD rats,Weight 250-300 g. Reference on Ishikawa N and Hamdy O establish the model of neurogenic pulmonary edema, then collected serum standby. In vitro culture of human pulmonary microvascular endothelial cell(HPMEC) were divided into 3 groups by randomly(control group, neurogenic pulmonary edema group, simvastatin group). Culture of 24 hours. Mtt colorimetry were performed to confirm cell apoptotic ratio; Flow cytometry was used to detected the apoptosis rate of HPMEC in these groups; Reverse transcriptase-polymerase chain reaction was used to detect the quantity of Bcl-2 m RNA and Bax m RNA; Western Blot was used to detect the expression level of Bcl-2 protein and Bax protein.Results:MTT:Compared with the neurogenic pulmonary edema group, simvastatin group of 24 h and 48 h increased the activity of cells(P<0.01).Flow cytometry : The average apoptosis rate of pulmonary microvascular endothelial cell in Control group is 4.28%, the average apoptosis rate of pulmonary microvascular endothelial cell in neurogenic pulmonary edema group is 35.96%, the average apoptosis rate of pulmonary microvascular endothelial cell in simvastatin group 16.98%. Compared with the control group, the apoptosis rate of neurogenic pulmonary edema group、simvastatin group is increased(P<0.01),but the neurogenic pulmonary edema group is increased more obviously; while the apoptosis rate of simvastatin group is decreased(P<0.01).RT-PCR : Compared with the control group, the neurogenic pulmonary edema group and simvastatin group, the m RNA of Bcl-2 and Bax expression levels were up-regulated(P<0.01). Compared with the neurogenic pulmonary edema group, simvastatin group the m RNA of Bcl-2 expression levels were up-regulated(P<0.01), while the m RNA of Bax expression levels were down-regulated(P<0.01).WB:Compared with the control group, the neurogenic pulmonary edema group and simvastatin group, the protein of Bcl-2 and Bax expression levels were up-regulated(P<0.01). Compared with the neurogenic pulmonary edema group, simvastatin group the protein of Bcl-2 expression levels were up-regulated(P<0.05), while the protein of Bax expression levels were down-regulated(P<0.01).Conclusions: Simvastatin can reduce the apoptosis of Human pulmonary microvascular endothelial cell, the underlying mechanism might be related to up regulation the expression of Bcl-2 and down regulation the expression of Bax.