1,3-二苯-1,3-丙二酮对硫代乙酰胺致小鼠急性肝损伤的保护作用

Protective effect of 1, 3-diphenyl-1, 3-propanedione for thioacetamide-induced liver injury in mice

目的:探讨1,3-二苯-1,3-丙二酮(DPPD)对硫代乙酰胺(TAA)致小鼠急性肝损伤的保护作用。方法:雄性ICR小鼠共40只,随机分为正常组、模型组和DPPD低、中、高剂量组,DPPD组分别灌胃给予DPPD 250,500和1 000 mg·kg-1·d-1,qd,给药4 d,正常组和模型组给予生理氯化钠溶液。d 4给予DPPD 0．5 h后,模型组和DPPD组腹腔注射TAA 80 mg·kg-1,正常组不染毒。所有动物均在染毒TAA 24 h后处死。分离血清,测定血清中丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)、乳酸脱氢酶(LDH)和碱性磷酸酶(ALP)的活性。留取部分肝组织用作常规病理切片检查;并取部分肝组织测定组织中还原型谷胱甘肽(GSH)和氧化型谷胱甘肽(GSSG)的含量。结果:与正常组比较,模型组小鼠血清ALT,AST,LDH和ALP活性均显著上升,GSH显著下降。与模型组比较,低、中、高剂量的DPPD组小鼠血清ALT,AST,LDH和ALP活性均显著降低,并呈剂量-依赖性,GSH显著上升。病理切片显示DPPD能够明显减轻TAA对肝组织的炎症性破坏。结论:DPPD对TAA引起的急性肝损害有一定的保护作用。

Objective：To evaluate the protective effect of 1,3-diphenyl-1,3-propanedione DPPD） for thioacetamide-induced acute liver injury. Methods：Forty male ICR mice were randomly assigned to normal control group, thioacetamide group （TAA） or one of three DPPD groups. Each DPPD group was dosed with DPPD 250, 500 or 1000 mg· kg^-1 daily, respectively, via oral gavage for 4 days. The control and TAA groups were supplemented with normal saline for 4 days. In the 4^th day, rats were i. p. given TAA 80 mg· kg^-1 30 min after the last DPPD administration in the TAA group and DPPD groups. The serum ALT, AST ALP and LDH activities of the rats were measured. The liver tissues were collected from euthanasic rats for the measurement of reduced glutathione and oxidized glutathione levels and the pathohistological evaluation. Results： Compared with the control group, the serum activities of ALT, AST, LDH and ALP were significantly increased, and the liver GSH level was significantly reduced in the TAA group. Compared with the TAA group, the serum activities of ALT, AST, LDH and ALP were significantly decreased, and the liver GSH level was significantly increased in a dose-dependent manner in the DPPD groups. The pathological examination showed less inflammatory damage of the liver tissues in the DPPD group than in the TAA group. Conclusion： DPPD had hepatoprotection from the thioacetamide-induced liver injury.