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糖原合成酶激酶-3抑制剂与1,6-二磷酸果糖联合应用对大鼠肝脏创伤的影响 被引量:1

Effects of combined use of glycogen synthase kinase-3 inhibitor and fructose-1, 6-diphosphate on liver trauma in rats
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摘要 目的探讨糖原合成酶激酶-3(glycogen synthase kinase-3,GSK-3)抑制剂和1,6-二磷酸果糖(fructose-1,6-diphosphate,FDP)联合应用对大鼠肝脏创伤救治的影响。方法健康SD大鼠49只,全部建立大鼠肝脏撞击破裂伤模型。先取42只大鼠按不同处理方式完全随机分为三组,即对照组(氯化钠组)、FDP组、FGI组(FDP+GSK-3抑制剂联合应用组)。三组再按处死取材时相点按随机数字表法平均分为缺血前组和再灌注4h组。剩余7只为再灌注4h时相点假手术组。测定各组血液中AST和ALT含量、肝组织糖原含量、SOD活力及MDA含量。结果缺血前肝脏糖原含量对照组〈FDP组〈FGI组(P〈0.01)。再灌注4h血液中ALT、AST含量对照组〉FDP组〉FGI组〉假手术组(P〈0.01),肝脏组织SOD活力对照组〈FDP组〈FGI组〈假手术组(P〈0.01);MDA含量对照组〉FDP组〉FGI组〉假手术组(P〈0.01)。结论联合应用GSK-3抑制剂和FDP能加强FDP对大鼠肝脏撞击破裂伤的保护作用,其机制可能与GSK-3抑制剂能在肝脏缺血前有效增强肝脏以FDP为底物的糖原合成作用,短时间内极大地增加肝脏糖原贮备,从而减轻大鼠创伤后肝脏的热缺血再灌注损伤有关。 Objective To investigate effects of combined use of glycogen synthase kinase (GSK) -3 inhibitor and fructose-1,6-diphosphate (FDP) on liver trauma in rats. Methods After creation of liver trauma model in 49 Sprague-Dawley rats, 42 rats were randomly divided into control group (NaCl group), FDP group and FGI Group (FDP and GSK-3 inhibitor in combination group). Then, each group was randomly subdivided into pre-ischemia group and 4-hour reperfusion group on account of time point when animals were sacrificed before and after ischemia. The other seven rats set as sham operation group (SH group) were sacrificed at 4-hour reperfusion time point. The AST and ALT levels in blood and glycogen content, SOD vitality and MDA content in liver tissues were determined. Results At pre-ischemia time point, liver glycogen content in three groups was in order of control group 〈 FDP group 〈 FGI group (P 〈0.01 ). At 4-hour reperfusion time point, blood ALT and AST levels in four groups were in order of control group 〉 FDP group 〉 FGI group 〉 SH group ( P 〈 0.01 ) ,while SOD vitality in liver tissues of four groups was in order of control group 〈 FDP group 〈 FGI group 〈 SH group ( P 〈 0. 01 ) and MDA content in four groups was in order of control group 〉 FDP group 〉 FGI group 〉 SH group ( P 〈 0. 01 ). Conclusions Combined use of FDP and GSK-3 inhibitor can enhance the protective effect of FDP on liver rupture, as may relate to the mechanism that GSK-3 inhibitor can effectively enhance glycogen synthesis of FDP as substrate before liver ischemia so that the liver glycogen storage is increased in a short period of time and hence post-traumatic warm ischemia-reperfusion injury is alleviated in the liver of rats.
出处 《中华创伤杂志》 CAS CSCD 北大核心 2010年第1期76-79,共4页 Chinese Journal of Trauma
基金 全军医学科学技术研究“十一五”计划专项资助项目(082012)
关键词 创伤和损伤 肝糖原 果糖二磷酸盐类 糖原合成酶激酶-3 再灌注损伤 Wounds and injuries, liver Liver glycogen Fructosediphosphates Glycogen synthase kinase-3 Reperfusion injury.
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