Effect of hydrogen sulfide, a new gaseous signal molecule, on pulmonary vascular smooth muscle cell apoptosis in rats
- VernacularTitle:新型气体信号分子硫化氢对低氧大鼠肺动脉平滑肌细胞凋亡的影响
- Author:
Xiaobo CHEN
;
Junbao DU
;
Chunyu ZHANG
;
Chaoshu TANG
;
Weijin ZHOU
;
- Publication Type:Journal Article
- Keywords:
Hydrogen sulfide;
Anoxia;
Hypertension, pulmonary;
Apoptosis
- From:
Journal of Peking University(Health Sciences)
2003;0(04):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the effects of hydrogen sulfide (H 2S) 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 2S 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 2S 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 2S 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 2S 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.
