摘要
目的:研究依那普利对四氯化碳(CCl4)所致急性肝损伤大鼠肝损伤和抗氧化功能的作用. 方法:将50只♂SD大鼠随机分为5组(每组10只):药物干预组(10mg/kg,5mg/kg和2.5mg/kg)、模型组和正常对照组,药物干预组和模型组均给予皮下注射CCl4(用等体积的橄榄油稀释),以制备急性肝损伤的大鼠模型,正常对照组用等体积的生理盐水注射,用高(10 mg/kg)、中(5 mg/kg)、低(2.5 mg/kg)剂量依那普利分别对SD大鼠灌胃给药.全自动生化分析仪测定大鼠血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、碱性磷酸酶(ALP)、胆汁酸(TBA)的活性;用比色分析法测定超氧化歧化酶(T-SOD)、黄嘌呤氧化酶(XOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性及丙二醛(MDA)的含量. 结果:依那普利显著降低因CCl4所致急性肝损伤大鼠血清ALT(正常对照组685±63 nkat/L<10 mg干预组1 241±168 nkat/L<5 mg干预组1 705±83 nkat/L<2.5 mg干预组2 302±174 nkat/L<模型对照组3 531±776 nkat/L),AST (正常对照组1 240±158nkat/L<10 mg干预组2 430±386 nkat/L<5 mg干预组2 788±522 nkat/L<2.5 mg干预组3 151±917 nkat/L<模型对照组3 372±138 nkat/L), ALP(10mg干预组2 567±159nkat/L<正常对照组2 659±248 nkatL<5 mg干预组3 212±198 nkat/L<2.5 mg干预组3 231±261 nkat/L<模型对照组3 609±346 nkat/L)和TBA(正常对照组8.48±0.49 μmol/L<10 mg干预组16.35±5.43μmol/L<5 mg干预组16.92±2.68 μmol/L<2.5 mg干预组17.53±3.59μmol/L<模型对照组24.16±9.27μmol/L) 的升高.对急性肝损伤大鼠血清GSH-PX(模型对照组50±54 nkat/L<2.5 mg干预组149±111 nkat/L<10 mg干预组169±141 nkat/L<5 mg干预组1 70±91 nkat/L<正常对照组295±194 nkat/L)的活性有明显的升高作用及降低T SOD(正常对照组6006±639 μkat/L<10mg干预组7 135±1 560μkat/L<2.5 mg干预组7 538±938 μkat/L<5 mg干预组7 589±780μkat/L<模型对照组8 579±861μkat/L) 和XOD(正常对照组571±28 nkat/L<10 mg干预组724±18nkat/L<5mg干预组821±28nkat/L<2.5mg干预组868±58 nkat/L<模型对照组1 042±188nkat/L)的含量.以上均与模型对照组比较aP<0.05,bP<0.01. 结论:依那普利的保肝机制和抗氧化作用与其对抗自由基脂质过氧化密切相关.
AIM: To investigate the effect of Enalpril on acute liver injury induced by carbon tetrachloride (CCl4) in rats and its anti-oxidative function. METHODS: Fifty normal male SD rats were randomly divided into five groups (10 rats/group): Enalpril interventional groups A, B, and C (10, 5, and 2.5 mg/kg, respectively), injury-model group, and control group. Rats in interventional and model groups were given hypodermic CCl4 (diluted with an eqal volume of olive oil). Rats in control group received normal saline injection. Rats with liver injury induced by CCL, were then treated with Enalpril (10, 5, 2.5; ig). The activities of serum aspartate transaminase (AST), a|a-nine transaminase (ALT), alkaline phosphatase (ALP) and total bile acid (TBA) were detected using full automatic biochemical analyzer. Superoxide dismutase (SOD), xan thine oxidase (XOD), glutathione perioxidase (GSH-PX), and malondialdehyde (MDA) were determined using colo rimetric method. RESULTS: Enalpril significantly reduced serum ALT (685±63, 1 241±168, 1 705±83, 2 302±174 nkat/L vs 3 531± 776 nkat/L in control, A, B, C versus model group respectively; P<0.01), AST (1 240±158, 2 430±386 nkat/L vs, 3 372± 138 nkat/L in control, A versus model group; P<0.01, P<0.05 respectively), ALP (2 659±248, 2 567±159 nkat/L vs3 609±346 nkat/L in control, A versus model group; P<0.01) and TBA (8.48±0.49, 16.35±5.43, 16.92± 2.68 μmol/L vs 24.16±9.27 μmol/L in control, A, B versus model group;P<0.01, P<0.05, P<0.05 respectively) in acute liver injury induced by CCI4. The level of XOD in model group was significantly higher than that in control, A, B and C groups (1 042±188 nkat/L vs 571±28, 724± 18, 821±28, 868±58 nkat/L; P <0.01). SOD level in model group was significantly higher than that in control and A group (8 579±861 nkat/L vs 6 006±639, 7 135± 1 560 nkat/L; P<0.01, P<0.05). MDA level in interventional group was obviously lower than that in model group and GSH-PX level was obviously higher than that in model group. CONCLUSION: Enalpril has protective effects for rats with acute hepatic injury induced by carbon tetrachloride and the mechanism closely relates to its anti-oxidative function.
出处
《世界华人消化杂志》
CAS
2004年第11期2638-2641,共4页
World Chinese Journal of Digestology
