银杏叶提取物抗氯化汞急性肾损伤的实验研究

Protective effect of Extract of Ginkgo Biloba against HgCl2-induced acute renal injury in Rats

目的探讨银杏叶提取物(EGb)能否诱导大鼠肾脏表达HO-1,减轻氯化汞所致的急性肾损伤。方法56只雄性Wistar大鼠随机分为Ⅰ组(腹腔注射EGb20mg/kg,24h后再注射HgCl21mg/kg)、Ⅱ组(腹腔注射EGb20mg/kg+ZnPPⅨ45μmol/kg,24h后再注射HgCl21mg/kg)、Ⅲ组(同时腹腔注射等量生理盐水+HgCl21mg/kg)、Ⅳ组(同时腹腔注射等量生理盐水+等量蒸馏水)。检测肾组织中HO-1蛋白表达及HO-1活力、丙二醛(MDA)含量、总抗氧化能力(TAOC)和血清肌酐(Cr)、尿素氮(BUN)含量并观察组织形态学改变。结果EGb明显诱导了肾内HO-1表达并增加其活力;与Ⅳ组比较,Ⅱ、Ⅲ组Cr、BUN、MDA升高,TAOC降低,组织学损伤严重(均P<0.05);与Ⅲ组比较,Ⅰ组染汞损伤前用EGb诱导HO-1表达,可逆转上述病理改变,而Ⅱ组用HO-1的抑制剂ZnPPⅨ后,则不能完全逆转上述病理改变。结论EGb能显著诱导肾内HO-1的表达并减轻HgCl2所致的急性肾损伤,其作用机制与HO-1增强肾组织抗氧化能力有关。

[Objective] To investigate whether Extract of Ginkgo Biloba （EGb） could induce heme oxygenase-1 （HO-1） in renal and attenuate the mercuric chloride （HgCl2）-induced acute renal injury in rats. [Methods] Fifty- six Wistar rats were randomly divided into four groups： group Ⅰ （rats were intraperitoneally injected with EGb 20 mg/ kg and 24 h later with 1 mg/kg HgCl2 ）, group Ⅱ （rats were injected with EGb 20 mg/kg ＋ ZnPPⅨ45 μmol/kg and then 1 mg/kg HgCl2）, group Ⅲ （rats were treated with equivalent volumes of saline and 1mg/kg HgCl2 at the same time） and groupⅣ （rats were given with equivalent volumes of saline and distilled water at the same time）. The expression of HO-1 and its activity in renal,serum levels of creatinine （Cr）, blood urea nitrogen（BUN）, tissue malondialdehyde （MDA） as well as total antl-oxldatlve capability （TAOC） were measured. [Results] （1） EGb induced the expression of HO-1 significantly and increased the HO activity markedly. （2） Compared with groupⅣ, the serum levels of Cr and BUN and MDA content were significandy higher and renal histologic damages showed more severe, but TAOC decreased dramatically in group m; induction of HO-1 by EGb before HgCl2 injection reversed the changes above, while the protective effect of EGb against HgCl2-induced acute renal injury was suppressed by HO- 1 inhibitor, Zinc protoporphyrin-Ⅸ （ZnPPⅨ）. [Conclusion] Our results indicated that EGb ameliorates HgCl2-in- duced acute renal injury in rats signlficandy by induction of HO-1.