HHI-I对大鼠肝缺血再灌注损伤的影响

Effects of Huoxue Huayu(活血化瘀) Injection-I on Liver Ischemia-Reperfusion Injury in Rats

目的:研究活血化瘀注射液I号(HHI-I)对大鼠肝脏缺血再灌注(IR)损伤的影响,并与缺血预处理(IP)比较作用的效果。方法:清洁级健康雄性SD大鼠80只,随机分为4组(Sham组,IR组,IP组,HHI-I组),测血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)的水平;取左肝测组织丙二醛(MDA)、超氧化物歧化酶(SOD)的含量。结果:IR组、IP组、HHI-I组的ALT、AST、LDH活性均明显高于Sham组(P<0·01),再灌注后SOD值均下降,各组各时间点与Sham组比较均具有统计学差异(P<0·05)。再灌注后MDA值均升高,缺血再灌注后6h升至最高点(P<0·01),且各时间点预处理组均低于IR组(P<0·05),HHI-I组MDA(3h、6h)明显低于IP组(P<0·05)。结论:大鼠肝脏缺血再灌注后造成了明显的肝脏损伤,IP与HHI-I预处理均可改善IR对肝脏造成的损伤,且后者效果优于前者。

Objective To study the effect of Huoxue Huayu（活血化瘀）Injection-1 （HHI- Ⅰ） on liver ischemia reperfusion（IR） injury in rats and compare them with ischemia preconditioning Methods Healthy adult male Sprague - Dawley rots were randomly divided into four groups： sham group（Sham）, Ischemia reperfusion group（IR）, ischemia preconditioning group（IP）, HHI- Ⅰ pretreatment group（HHI- Ⅰ）. Partial hepatic ischemia and reperfusion model was made. HHI - Ⅰ group rots were administered HHI - Ⅰ（ 10 ml/kg h. w. ） by penis vein 5 minutes before liver ischemia. Rats from each group were sacrificed to determine serum AST （alanine aminotransferase）, ALT（alnine aminotransferase）, LDH（lactate dehydrogenase）, MDA（malondialdehyde）, SOD（superoxide dismutase） level at the four time points 1, 3,6 and 24 hour of reperfusion, respectively. Histologic and ultra - structune changes of the liver were observed after 3 hours of reperfusion. Results IR caused significant increase in serum AST, ALT, LDH, and liver tissue MDA level. Liver tissue SOD level was significantly reduced in the IR group than that in sham group, but SOD levels in the HHI- Ⅰ group and IP group were higher than that in IR group. As compared with the IR group, animals treated with HHI - Ⅰ or IP expressed a significant decrease in serum AST, ALT, and tissue LDH level in all reperfusion periods.Sermn AST, LDH（in all reperfusion periods）, ALT（at lh, 6h, 24h after reperfusion） and tissue MDA（at 3h, 6h after reperfusion） levels in animals receiving HHI- Ⅰ were significantly reduced as compared with those of receiving ischemia preconditioning animals. Liver injury in the HHI-Itreated animals and IP treated animals were attenuated compared with that in the IR group. Conclusion HHI - Ⅰ pretreatment can induce liver tolerance to warm IR in rots just as IP, showing a preventive effect on hepatic ischemia reperfusion injury by elimination of oxygen tree radical and the subsequent suppression of lipid peroxidation.