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作 者:安伟[1] 刘军[1] 管冬诗[1] 杨凤辉[1] 许世峰[1] 周旭[1]
机构地区:[1]山东大学附属省立医院器官移植中心肝胆外二科,山东济南250021
出 处:《中国普通外科杂志》2010年第1期32-36,共5页China Journal of General Surgery
基 金:山东省优秀中青年奖励基金资助项目(2005BS03006)
摘 要:目的探讨姜黄素预处理对大鼠肝脏冷缺血再灌注损伤(IRI)的保护作用及其机制。方法将40只Wistar大鼠随机分为:实验组(21只),于术前2 h将60 mg/kg的姜黄素溶于1mL DMSO中静脉注射;对照组(19只),于术前2h静脉注射1 mL DMSO。肝脏冷灌注时间为30 min,恢复血供复流6 h后处死动物,留取血液和肝脏标本,行血清ALT,AST,LDH和组织匀浆SOD,MDA,MPO测定,并进行组织病理和细胞凋亡检测。酶联免疫吸附试验(ELISA)检测肝组织匀浆中TNF-α及MIP-2的水平变化。结果实验组大鼠血清ALT,AST,LDH水平明显低于对照组(P<0.01);实验组MDA,MPO,TNF-α和MIP-2水平较对照组明显降低(P<0.05),SOD含量较对照组明显增高(P<0.05)。并且实验组大鼠肝组织损伤程度和细胞凋亡程度明显轻于对照组。结论姜黄素预处理能减轻大鼠肝脏冷IRI,其保护机制可能与提高肝组织SOD含量,抑制脂质过氧化与细胞凋亡,下调炎性因子TNF-α和MIP-2的表达以及减少中性粒细胞浸润有关。Objective To investigate the protective effect of curcumin in hepatic cold ischemia-reperfusion injury in rats and its possible mechanisms.Methods Forty Wistar rats were randomly divided into two groups: the experimental group(n=21),rats were administered curcumin by injection through tail vein at the dose of 60mg/kg which was dissolved in one milliliter DMSO two hours before cold ischemia period,and the remaining rats served as control group.The hepatic cold ischemia was 30 minutes.All the rats were sacrificed six hours after reperfusion.Blood and liver samples were collected for determination of serum levels of ALT,AST and LDH and the tissue homogenate levels of SOD,MDA and MPO.Pathomorphological changes of liver tissue and the situation of apoptosis were observed under optical microscope.The content of TNF-α and MIP-2 in the liver homogenate were determined by enzyme linked immunosorbent assay(ELISA).Results Compared with control groups,the serum levels of ALT,AST and LDH in experimental groups were significantly decreased(P0.01).The tissue homogenate levels of MDA,MPO,TNF-α and MIP-2 in experimental groups were significantly decreased.(P0.05);the level of SOD was obviously elevated(P0.05).Pathological studies indicated that curcumin attenuated liver tissue injury and inhibited apoptosis in the rats.Conclusions Curcumin can attenuate the cold ischemia-reperfusion injury of liver in rats,and its possible mechanisms may be related to increasing the activity of SOD,inhibiting lipid peroxidation and apoptosis,decreasing the expression of TNF-α and MIP-2,and suppressing the activation and infiltration of neutrophils.
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