Sulforaphane protects liver injury induced by intestinal ischemia reperfusion through Nrf2-ARE pathway
Sulforaphane protects liver injury induced by intestinal ischemia reperfusion through Nrf2-ARE pathway作者机构：Dalian Med Univ Affiliated Hosp 2 Dept Gen Surg Dalian 116023 Liaoning Prov Peoples R China Dalian Med Univ Dept Pharmacol Dalian 116044 Liaoning Prov Peoples R China
出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)
年 卷 期：2010年第16卷第24期
页 面：3002-3010页
核心收录：
学科分类：1002[医学-临床医学] 1001[医学-基础医学(可授医学、理学学位)] 100104[医学-病理学与病理生理学] 10[医学]
基 金：Supported by The grants of Chinese National Natural Science Foundation, No. 30872449 the grants of the Dalian Scientific Research Foundation, No. 2008E13SF217
主 题：Sulforaphane Liver injury Intestinal isch-emia reperfusion NF-E2-related factor-2 Antioxidant response element
摘 要：AIM: To investigate the effect of sulforaphane (SFN) on regulation of NF-E2-related factor-2 (Nrf2)-antiox-idant response element (ARE) pathway in liver injury induced by intestinal ischemia/reperfusion (I/R). METHODS: Rats were divided randomly into four ex-perimental groups: control, SFN control, intestinal I/R and SFN pretreatment groups (n = 8 in each group). The intestinal I/R model was established by clamping the superior mesenteric artery for 1 h and 2 h reperfu-sion. In the SFN pretreatment group, surgery was performed as in the intestinal I/R group, with intraperitoneal administration of 3 mg/kg SFN 1 h before the op-eration. Intestine and liver histology was investigated. Serum levels of aspartate aminotransferase (AST), and alanine aminotransferase (ALT) were measured. Liver tissue superoxide dismutase (SOD), myeloperoxidase (MPO), glutathione (GSH) and glutathione peroxidase (GSH-Px) activity were assayed. The liver transcription factor Nrf2 and heme oxygenase-1 (HO-1) were determined by immunohistochemical analysis and Western blotting ***: Intestinal I/R induced intestinal and liver injury, characterized by histological changes as well as a signif icant increase in serum AST and ALT levels (AST: 260.13 ± 40.17 U/L vs 186.00 ± 24.21 U/L, P 0.01; ALT: 139.63 ± 11.35 U/L vs 48.38 ± 10.73 U/L, P 0.01), all of which were reduced by pretreatment with SFN, respectively (AST: 260.13 ± 40.17 U/L vs 216.63 ± 22.65 U/L, P 0.05; ALT: 139.63 ± 11.35 U/L vs 97.63 ± 15.56 U/L, P 0.01). The activity of SOD in the liver tissue decreased after intestinal I/R (P 0.01), which was enhanced by SFN pretreatment (P 0.05). In ad-dition, compared with the control group, SFN markedly reduced liver tissue MPO activity (P 0.05) and elevat-ed liver tissue GSH and GSH-Px activity (P 0.05, P 0.05), which was in parallel with the increased level of liver Nrf2 and HO-1 ***: SFN pretreatment attenuates liver injury induced by intestinal I
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