[Effect of hydrogen sulfide, a new gaseous signal molecule, on pulmonary vascular smooth muscle cell apoptosis in rats].
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.


CONCLUSIONS
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.
Chen
Xiao-bo
XB
Department of Pediatrics, Peking University First Hospital, Beijing 100034, China.
Du
Jun-bao
JB
Zhang
Chun-yu
CY
Tang
Chao-shu
CS
Zhou
Wei-jin
WJ
D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D053148:Caspase 3 / Q000096:biosynthesis; D006862:Hydrogen Sulfide / Q000097:blood / Q000494:pharmacology*; D000860:Hypoxia / Q000503:physiopathology; D007150:Immunohistochemistry; D020287:In Situ Nick-End Labeling; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000096:biosynthesis; D011651:Pulmonary Artery / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D013053:Spectrophotometry / Q000379:methods; D019014:fas Receptor / Q000096:biosynthesis
D019253:Proto-Oncogene Proteins c-bcl-2; D019014:fas Receptor; D053148:Caspase 3; D006862:Hydrogen Sulfide