18α、18β-甘草酸及其不同配比物对CCl_4肝损伤大鼠的影响

Influence of 18-α,18 β-Glycyrrhizic Acids and their Different Proportions on CCl_4 Hepatotoxicity in Rats

目的:研究不同配比的18α、18β-甘草酸(GL)对四氯化碳(CCl4)肝损伤大鼠的保护作用,探讨临床应用合理比例。方法取健康雄性SD大鼠(200±20)g 70只,随机分为7组,即正常组、CCl4肝损伤组、18α-GL、18β-GL和3个不同配比组(α:β比例分别为4∶6、3∶7和2∶8)。采用腹腔注射CCl4复制大鼠急性肝损伤模型。分别于24h和48h后摘眼球取血,测定血清谷丙转氨酶(ALT)、谷草转氨酶(AST)、乳酸脱氢酶(LDH)活性,同时测定肝脾重量,肝脏超氧化物歧化酶(SOD),并对肝细胞的组织形态学进行观察。结果:模型组大鼠ALT、AST、肝脏系数显著增高,脾脏系数和SOD活性显著降低,组织病理学亦有显著差异,造模成功。5个药物组中以18α-和18β-GL配比为3∶7最佳,能显著抑制CCl4引起的大鼠血清ALT、AST及肝脏系数的升高以及脾脏系数和肝脏SOD活性的降低,并能显著减轻CCl4引起的肝细胞组织病理学改变。结论:18α-与18β-GL 3∶7配比组对CCl4致大鼠肝损伤具有较强的保护作用。

Objective： To study the protective function and select the optimal formulation of 18α,18β-glycyrrhizic acid and their different proportions against CC14induced hepatotoxicity in rats. Methods：Healthy SD male rats, weighting （200±20）g, 10 per group were randomized into 7 groups： control group, CC14 -injured group, 18α-glycyrrhizie acid group, 18β - glycyrrhizic acid group and their proportions of 4 ： 6, 3 ： 7, 2 ： 8 groups. 6% CCl4 was given to rats by intra-peritoneal （ip） injection, with the exception of control group. The rats were killed 24 h and 48h after CCl4 injury respectively. Serum alanine amiotransferase （ALT） ,aspartate aminotransferase （AST） and lactate dehydrogcnase （LDH） activities were determined; the liver and spleen weights of each rat as well as superoxide dismutase （SOD） activity in the liver homogenatc were also detected. The liver pathological examination was also judged. Results ：The acute CCl4 - injured model was successfully established due to increased serum enzyme level, swollen liver, atrophied spleen, decreased SOD activity and change in liver pathological examination Among the five formulations, the 3 ： 7 group did best in inhibiting the increases of serum ALT, AST and liver index, preventing the decreases of spleen index and SOD activity, and alleviating the lesion in liver cell obviously. Conclusion ： In all, the formulation of 3 ： 7 showed the most potent liver protection against CCl4 - induced hepatotoxicity.