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＊Ｐ＜０．００１从表３可见，ＣｏＱ１０高低剂量组肝匀浆ＣｙｔＰ４５０含量与ｎＳ对照组比较没有明显差异（Ｐ＞０．０５），而苯巴比妥钠组小鼠肝匀浆ＣｙｔＰ４５０含量较ＮＳ对照组及高低剂量组显著升高，有非常显著性差异（Ｐ＜０．００１）。本巴比妥钠为肝药酶诱导剂，其阳性结果证明此实验方法可靠，也证明ＣｏＱ１０对肝细胞ＣｙｔＰ４５０含量没有影响。３讨论本实验结果表明：小鼠用ＣｏＱ１０作预处理，确能保护超量ＡＡＰ对肝脏的损伤作用；同时能使ＡＡＰ血清浓度明显升高，而对肝细胞ＣｙｔＰ４５０含量则无影响。据文献报道，超ｔＡＡＰ进入肝细胞微粒体后，通过肝药酶代谢产出大量毒性中间产物，因而引起肝损害甚至肝坏死［７］。ＣｏＱ１０能防止这一毒性效应，通过稳定肝细胞微粒体膜或抑制肝药酶活住，均可达此目的．上述实验结果．均提示ＣｏＱ１０的作用途径可能是稳定肝细胞微粒体膜，使ＡＡＰ进入微粒体数量减少，因而毒性中间代射产物生成减少，使肝细胞损伤减轻。参考文献
* P <0.001 As can be seen from Table 3, CytP450 content in the homogenate CoQ10 high and low dose group had no significant difference compared with the nS control group (P> 0.05), while the content of CytP450 in the liver homogenate of the phenobarbital sodium group Compared with the NS control group and the high and low dose groups, there was a significant difference (P <0.001). The barbital sodium hepatic drug inducer, the positive results prove that this experimental method is reliable, also proved CoQ10 hepatocyte CytP450 content has no effect. 3 Discussion The experimental results show that: mice pretreatment with CoQ10 indeed protects against excessive AAP damage to the liver; while AAP serum concentration was significantly increased, while the content of CytP450 hepatocytes had no effect. It has been reported in the literature that after super tAAP enters hepatocyte microsomes, a large amount of toxic intermediate products are produced through hepatic enzyme metabolism, thereby causing liver damage and even hepatic necrosis [7]. CoQ10 can prevent this toxic effect, by stabilizing the membrane of liver cell microsomes or inhibiting hepatic drug live, can achieve this goal. The above experimental results. Both suggest that the mechanism of action of CoQ10 may be to stabilize the liver cell microsome membrane, so that the number of AAP into the microsome decreases, so the generation of toxic intermediates to reduce the generation of products to reduce liver cell damage. references