论文部分内容阅读
[目的]研究葛根素对兔缺血再灌注损伤中肝脏能量代谢的改善作用及其机制。[方法]将30只家兔随机均分为对照组(C组)、缺血/再灌注组(IR组)和葛根素组(Pur组)。测定血浆中谷丙转氨酶(ALT)浓度和肝组织内一磷酸腺苷(AMP)、二磷酸腺苷(ADP)、三磷酸腺苷(ATP)、总腺苷酸量(TAN)、肝脏的细胞能荷(EC)、丙二醛(MDA)、超氧化物歧化酶(SOD)、一氧化氮(NO)、内皮素(ET)、NO/ET、血栓素B2(TXB2)、前列腺素F1α(PGF1α)、TXB2/PGF1α水平,并观察肝细胞形态学的改变。[结果]与C组比较,IR组血浆ALT浓度、肝组织AMP、ADP、MDA、ET含量显著升高(P<0.01),TXB2、TXB2/PGF1α亦明显升高(P<0.05),肝组织ATP、EC、SOD、NO/ET显著下降(P<0.01),NO、PGF1α亦明显降低(P<0.05),TAN差异无统计学意义(P>0.05),肝细胞形态学异常改变;与IR组比较,Pur组血浆ALT浓度、肝组织AMP、MDA、ET含量显著降低(P<0.01),肝组织ADP、TXB2/PGF1α亦明显减少(P<0.05),TXB2略低于IR组(P>0.05),肝组织ATP、EC、SOD、NO/ET显著升高(P<0.01),肝组织NO、PGF1α亦明显增高(P<0.05),TAN差异无统计学意义(P>0.05),肝细胞形态学异常改变较大程度减轻。[结论]葛根素(60mg/kg)预处理可通过拮抗氧化损伤、调节NO/ET和前列腺素I2/血栓素A2(PGI2/TXA2)失衡而改善肝细胞的能量代谢,有效防治兔肝再灌注损伤。
[Objective] To study the effect of puerarin on hepatic energy metabolism in ischemia-reperfusion injury in rabbits and its mechanism. [Method] Thirty rabbits were randomly divided into control group (C group), ischemia / reperfusion group (IR group) and puerarin group (Pur group). The concentrations of ALT and ADP, ADP and TAN in the liver were measured. The EC of the liver (EC ), MDA, SOD, NO, ET, NO / ET, TXB2, PGF1α, TXB2 / PGF1α levels, and observe the morphological changes of hepatocytes. [Results] Compared with group C, the levels of plasma ALT, the content of AMP, ADP, MDA and ET in liver tissue of IR group were significantly increased (P <0.01), TXB2 and TXB2 / PGF1α were also significantly increased (P <0.01), NO and PGF1α also decreased (P <0.05), TAN showed no significant difference (P> 0.05) (P <0.01), the levels of ADP and TXB2 / PGF1α in liver decreased significantly in Pur group (P <0.05), while the levels of TXB2 in hepatic tissue were lower than those in IR group (P> 0.05). The levels of NO, PGE1 and NO in liver increased significantly (P <0.01) and the levels of NO, PGF1α in liver increased significantly (P <0.05) Abnormal changes in cell morphology to a greater extent alleviate. [Conclusion] Puerarin (60 mg / kg) pretreatment can improve the energy metabolism of hepatocytes by antagonizing the oxidative damage, regulating the imbalance of NO / ET and PGI2 / TXA2, and effectively prevent and cure the reperfusion of rabbit liver damage.