黄芪总苷和三七总皂苷配伍对小鼠脑缺血再灌注脑组织能量障碍的影响

目的探讨黄芪总苷(AST)和三七总皂苷(PNS)对脑缺血再灌注小鼠能量代谢障碍的影响。方法 C57BL/6小鼠被随机分成假手术组、模型组、AST组(110 mg/(kg.d),ig),PNS组(115 mg/(kg.d),ig),AST+PNS配伍组(AST110 mg/(kg.d)+PNS 115 mg/(kg.d),ig)和依达拉奉组(8 mg/(kg.d),ip),分别给药,连用4 d。在最后1次给药1 h后制作脑缺血再灌注损伤模型,检测脑组织三磷酸腺苷(ATP)、二磷酸腺苷(ADP)、一磷酸腺苷(AMP)含量和Na+-K+-ATPase酶活性。结果 AST和PNS配伍对脑缺血再灌注后ATP、ADP含量、总腺苷酸池(TAN)值和ATP酶活性的降低具有协同抑制作用,差异具有统计学意义(P<0.01),对能荷(EC)值的减少具有相加的抑制作用(P<0.05)。结论 AST和PNS配伍可以明显改善脑缺血在灌注后能量代谢障碍,其作用机制可能与AST和PNS能协同提高脑组织能量的利用和生成,改善能荷、增强Na+-K+-ATPase的活性有关。

Effects of Astragalosides and Panax notoginseng saponins combination on energy metabolism of brain tissues after cerebral ischemia-reperfusion in mice

Objective To investigate the effects of Astragalosides（AST） and Panax notoginseng saponins （PNS） combination on energy metabolism disturbance after cerebral ischemia-reperfusion in mice. Methods C57BL/6 mice were randomly divided into 6 groups as follows： sham-operat- ed group,model group,Astragalosides group（AST, 110 mg/kg·d,ig）,Panax notoginseng saponins group （PNS,115 mg/kg·d,ig） ,AST combined with PNS group （AST 110 mg/kg-d＋PNS 115 mg/kg·d,ig） and 3-methyl-l-phenyl-2-pyrazoline-5-one group （edaravone,8 mg/kg·d,ip）. All mice were admin- istered respectively and lasted for 4 d. After the last treatment for 1 h,cerebral ischemia-reperfu- sion injury model was established. Then, the contents of adenylate（ATP,ADP,AMP） in brain tissues were measured and the activities of Na＋-K＋-ATPase were evaluated. Results AST combined with PNS exhibited synergistic inhibition effects on the decrease of ATP and ADP contents, total adenine nucleotides （TAN） and ATPase activities （all P〈0.01）,and exhibited addition inhibition effects on the decrease of energy charge （EC） （P〈0.05）. Conclusion These results AST combined with PNS significantly improve cerebral energy metabolism dysfunc suggest that tion after is- chemia-reperfusion. The underlying mechanism may be that AST and PNS synergistically promote the supply and generation of energy, improve the energy charge, enhance Na＋-K＋-ATPase activity in brain tissues.