Objective: To explore the effects of hydrogen sulfide (H(2)S) on hypoxic pulmonary vascular smooth muscle cell (VSMC) apoptosis in rats.
Methods: Twenty-four Wistar rats were divided into 3 groups: control group (n=8), hypoxia group (n=8), and hypoxia +NaHS group (n=8). The plasma level of H(2)S was determined by methylene blue spectrophotometric method. VSMC apoptosis was measured by terminal deoxynucleotidyl transferase-biotin nick end labeling (TUNEL). The protein expressions of Bcl-2, Fas and caspase-3 in pulmonary arteries were detected by immunohistochemical technique.
Results: Compared with rats in the control group, the plasma level of H(2)S decreased by 36% in rats of hypoxic group. The apoptotic rate per area in VSMCs detected with TUNEL was significantly decreased by 52.9% in rats of hypoxic group. The expressing integral score of Bcl-2 of VSMCs was increased by 123.9% while Fas protein expression of VSMCs was decreased by 45% and caspase-3 protein expression of VSMCs was not significantly changed in rats of hypoxia group. But compared with rats in the hypoxia group, the plasma level of H(2)S increased by 65% in rats of hypoxia+NaHS group. The apoptotic rate in VSMCs of TUNEL was significantly increased by 62.5% in rats of hypoxia+NaHS group. The Bcl-2 protein expression of VSMCs was decreased by 36.4% in rats of hypoxia+NaHS group. The expressing integral scores of Fas and caspase-3 were significantly higher in rats of hypoxia+NaHS group than in those of hypoxia group.
Conclusion: Hypoxia decreased the pulmonary artery smooth muscle cell apoptosis. H(2)S inhibited Bcl-2 protein expression of VSMCs and activated Fas and caspase-3 protein expressions of VSMCs, and therefore promoted the pulmonary artery smooth muscle cell apoptosis.
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