Protective Effects of Ischemic Postconditioning on Liver Oxidative Stress in a Rat Model of Laparoscopic Pneumoperitoneum
Sun Qing-lin
Abstract
Sun Qing-lin
Abstract
Objective To investigate the protective effects of ischemic postconditioning on liver oxidative stress in a rat model of laparoscopic pneumoperitoneum(P).Method Twenty-four male SD rats were randomly divided into 4 groups,the pneumoperitoneum(group P),ischemic preconditioning(group IP),ischemic postconditioning(group IPo) and control(group C).Animals in the group C was subjected to sham operation,in the other groups were subjected to the CO2 pneumoperitoneum,15mm Hg intra-abdominal pressure(IAP).P group was subjected to 60 min of P,followed by 30 min of deflation(D),IP group was subjected to preconditioning prior to P/D,which consisted of 10 min of P,followed by 10 min of D,IPo group was subjected to 60 min of P,followed by three cycles of 1 min of D and 1 min of P and 30 min of D.Plasma alanine aminotransferase(ALT) and aspartate aminotransferase(AST),as well as homogenized tissue malondialdehyde(MDA) and nitric oxide(NO) levels,glutathione(GSH) activities were measured.The expression of iNOS in liver tissue was examined by immunohistochemical technique in each group.Results Plasma ALT and AST as well as liver MDA levels significantly increased in groups P,IP and IPo,as compared to those in group C(P0.05).Plasma ALT,AST as well as liver MDA and NO levels significantly decreased,whereas liver GSH values increased in groups IP and IPo,as compared to group P(P0.05).The biochemical markers except GSH were no significantly different be-tween group IP and IPo.The iNOS concentration markedly decreased in group IPo in comparison with group P.Conclusions Ischemic postconditioning can increase GSH levels and inhibit the expression of iNOS that can induce the production of NO,which may decrease hepatic oxidative stress induced by CO2 pneumoperitoneum.Compared with IP,IPo increased GSH more prominently.It is suggested that IPo may play a greater role as protective effect on oxidative stress.
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Objective To investigate the protective effects of ischemic postconditioning on liver oxidative stress in a rat model of laparoscopic pneumoperitoneum(P).Method Twenty-four male SD rats were randomly divided into 4 groups,the pneumoperitoneum(group P),ischemic preconditioning(group IP),ischemic postconditioning(group IPo) and control(group C).Animals in the group C was subjected to sham operation,in the other groups were subjected to the CO2 pneumoperitoneum,15mm Hg intra-abdominal pressure(IAP).P group was subjected to 60 min of P,followed by 30 min of deflation(D),IP group was subjected to preconditioning prior to P/D,which consisted of 10 min of P,followed by 10 min of D,IPo group was subjected to 60 min of P,followed by three cycles of 1 min of D and 1 min of P and 30 min of D.Plasma alanine aminotransferase(ALT) and aspartate aminotransferase(AST),as well as homogenized tissue malondialdehyde(MDA) and nitric oxide(NO) levels,glutathione(GSH) activities were measured.The expression of iNOS in liver tissue was examined by immunohistochemical technique in each group.Results Plasma ALT and AST as well as liver MDA levels significantly increased in groups P,IP and IPo,as compared to those in group C(P0.05).Plasma ALT,AST as well as liver MDA and NO levels significantly decreased,whereas liver GSH values increased in groups IP and IPo,as compared to group P(P0.05).The biochemical markers except GSH were no significantly different be-tween group IP and IPo.The iNOS concentration markedly decreased in group IPo in comparison with group P.Conclusions Ischemic postconditioning can increase GSH levels and inhibit the expression of iNOS that can induce the production of NO,which may decrease hepatic oxidative stress induced by CO2 pneumoperitoneum.Compared with IP,IPo increased GSH more prominently.It is suggested that IPo may play a greater role as protective effect on oxidative stress.
Key concepts: Pneumoperitoneum, Malondialdehyde, Oxidative stress, Glutathione, Nitric oxide, Medicine, Internal medicine, Endocrinology