Sympathetic nervous system mediates surgical trauma stress-induced splenocyte apoptosis in rats.
Surgical trauma stress has been reported to induce immunosuppression. The mechanisms involved are still unclear. The present study was designed to assess the role of the sympathetic nervous system in regulating splenocyte apoptosis induced by surgical trauma stress. Our results showed that the rats that underwent surgical trauma stress exhibited a significant reduction in splenic cellularity, the loss of splenocytes was likely mediated by apoptosis, for a substantial increase in apoptosis was observed by using DNA gel electrophoresis and TUNEL assay. At the same time, an increase in Fas(CD95/Apo-1) protein expression in splenocytes was also observed. These effects were significantly abolished by either chemical sympathectomy or beta-adrenergic receptor antagonist propranolol. The data clearly revealed that the sympathetic nervous system especially beta-adrenergic receptors was involved in surgical trauma-induced immune alterations via a mechanism of apoptotic cell death.
Wang
Jun
J
Department of Integrative Medicine and Neurobiology, Shanghai Medical College, Fudan University, and Department of Pathology, Chang Zheng Hospital, Shanghai, 200032, China.
Sun
Jing
J
Yu
Jin
J
Cao
Xiao-Ding
XD
Wang
Yan-Qing
YQ
Wu
Gen-Cheng
GC
D000818:Animals; D017209:Apoptosis; D020287:In Situ Nick-End Labeling; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000166:cytology / Q000473:pathology*; D013312:Stress, Physiological / Q000276:immunology*; D013514:Surgical Procedures, Operative; D013564:Sympathetic Nervous System / Q000502:physiology*