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目的研究急性乙醇中毒对大鼠肝功能及组织病理学的影响及葛根素的保护作用。方法 Wistar大鼠分为对照组、模型组、葛根素组;染毒5 d后,检测各组血清及肝组织匀浆GST、MDA含量,并于普通光镜及电镜下观察肝组织病理学改变。结果模型组大鼠营养状态差,肝组织出现浊肿、脂变、局灶性坏死,肝糖原减少、线粒体增大畸形及嵴断裂,细胞器明显减少;血清MDA、GST水平分别为(9.60±2.99)nmol/ml、(33.17±9.79)U/ml,肝组织匀浆MDA、GST水平分别为(5.87±2.09)nmol/mg protein、(75.47±11.44)U/mg protein,均较对照组显著升高(P<0.05,P<0.01);葛根素组大鼠营养状态尚可,肝组织损伤较模型组明显减轻,血清MDA、GST水平分别为(6.63±1.96)nmol/ml、(23.69±5.40)U/ml,肝组织匀浆MDA、GST水平分别为(3.85±1.13)nmol/mg protein、(64.80±6.11)U/mg protein,均较模型组明显降低(P<0.05)。结论急性乙醇中毒可致大鼠肝功能异常,并引起急性肝病理学改变;葛根素可通过拮抗脂质过氧化等机制对急性乙醇中毒所致肝损伤起到一定保护作用。
Objective To investigate the effect of acute alcoholism on liver function and histopathology in rats and the protective effect of puerarin. Methods Wistar rats were divided into control group, model group and puerarin group. After 5 d of exposure, the content of GST and MDA in serum and liver homogenate of each group were detected. The pathological changes of liver tissue were observed under ordinary light and electron microscope . Results The rats in model group had poor nutrition status, turbidity, fat loss, focal necrosis, decreased hepatic glycogen, enlarged mitochondria, degeneration of cristae and organelles. The levels of MDA and GST in serum were (9.60 ± 2.99) nmol / ml and (33.17 ± 9.79) U / ml respectively. The levels of MDA and GST in liver homogenate were (5.87 ± 2.09) nmol / mg protein and (75.47 ± 11.44) U / mg protein respectively (P <0.05, P <0.01). The rats in puerarin group had a good nutrition status and the liver injury was significantly reduced compared with model group. The levels of serum MDA and GST were (6.63 ± 1.96) nmol / ml and (23.69 ± 5.40) U / ml, respectively. The level of MDA and GST in liver homogenate were (3.85 ± 1.13) nmol / mg protein and (64.80 ± 6.11) U / mg protein respectively, which were significantly lower than those in model group (P <0.05). Conclusions Acute ethanol intoxication can cause abnormal liver function in rats and lead to acute liver pathological changes. Puerarin can play a protective role against liver injury induced by acute alcohol poisoning by antagonizing lipid peroxidation and other mechanisms.