机构地区:[1]Department of Pharmacology, Dalian Medical University, Dalian 116044, Liaoning Province, China [2]Department of Heneral Surgery, Second Affiliated Hospital of Dalian Medical University, Dalian 116023, LiaoningProvince, China [3]Department of Hepatobiliary and Pancreatic Surgery, First Affiliated Hospital, Zhejiang University Schoolof Medicine, Hangzhou 310003, Zhejiang Province, China
出 处:《World Journal of Gastroenterology》2009年第26期3240-3245,共6页世界胃肠病学杂志(英文版)
基 金:Supported by The grants from the Dalian Scientific Research Foundation,No.2004 B3SF 143,No.2007 J21JH006;National Natural Science Foundation,No.30872449
摘 要:AIM: To investigate the possible protective effects of carnosol on liver injury induced by intestinal ischemia reperfusion (I/R). METHODS: Rats were divided randomly into three experimental groups: sham, intestinal I/R and carnosol treatment (n = 18 each). The intestinal I/R model was established by clamping the superior mesenteric artery for 1 h. In the carnosol treatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg carnosol 1 h before the operation. At 2, 4 and 6 h after reperfusion, rats were killed and blood, intestine and liver tissue samples were obtained. Intestine and liver histology was investigated. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and interleukin (IL)-6 were measured. Liver tissue superoxide dismutase (SOD) and myeloperoxidase (IvIPO) activity were assayed. The liver intercellular adhesion molecule-1 (ICAM-1) and nuclear factor κB (NF-κB) were determined by immunohistochemical analysis and western blot analysis. RESULTS: Intestinal I/R induced intestine and liver injury, characterized by histological changes, as well as a significant increase in serum AST and ALT levels. The activity of SOD in the liver tissue decreased after I/R, which was enhanced by carnosol pretreatment. In addition, compared with the control group, carnosol markedly reduced liver tissue MPO activity and serum IL-6 level, which was in parallel with the decreased level of liver ICAI-1 and NF-κB expression. CONCLUSION: Our results indicate that carnosol pretreatment attenuates liver injury induced by intestinal I/R, attributable to the antioxidant effect and inhibition of the NF-κB pathway.AIM:To investigate the possible protective effects of carnosol on liver injury induced by intestinal ischemia reperfusion (I/R). METHODS: Rats were divided randomly into three experimental groups:sham, intestinal I/R and carnosol treatment (n=18 each). The intestinal I/R model was established by clamping the superior mesenteric artery for 1h. In the carnosol treatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg carnosol 1h before the operation. At 2, 4 and 6h after reperfusion, rats were killed and blood, intestine and liver tissue samples were obtained. Intestine and liverhistology was investigated. Serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT) and interleukin (IL)-6 were measured. Liver tissue superoxide dismutase (SOD) and myeloperoxidase (MPO) activity were assayed. The liver intercellular adhesion molecule-1 (ICAM-1) and nuclear factor κB (NF-κB) were determined by immunohistochemical analysis and western blot analysis. RESULTS: Intestinal I/R induced intestine and liver injury, characterized byhistological changes, as well as a significant increase in serum AST and ALT levels. The activity of SOD in the liver tissue decreased after I/R, which was enhanced by carnosol pretreatment. In addition, compared with the control group, carnosol markedly reduced liver tissue MPO activity and serum IL-6 level, which was in parallel with the decreased level of liver ICAM-1 and NF-κB expression. CONCLUSION: Our results indicate that carnosol pretreatment attenuates liver injury induced by intestinal I/R, attributable to the antioxidant effect and inhibition of the NF-κB pathway.
关 键 词:CARNOSOL Liver injury Ischemia reperfusion Nuclear factor κB
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