摘要
目的:观察1,3-二苯-1,3-丙二酮(1,3-diphenyl-1,3-propanedione,DPPD)对四氯化碳(CCl4)致小鼠急性肝损伤的保护作用。方法:将雄性ICR小鼠ig给予DPPD 4d,剂量分别为125,250,500和1 000 mg·kg-1·d-1,d4给予DPPD 0.5 h后,皮下注射CCl4染毒造模。染毒24 h后,内眦取血,测定血清中丙氨酸转移酶(ALT)、天冬氨酸转移酶(AST)和乳酸脱氢酶(LDH)的活性。留取动物肝脏组织,观察肝脏病理变化并测定肝脏组织内谷胱甘肽(GSH)和氧化型谷胱甘肽(GSSG)含量。结果:与模型组比较,DPPD各剂量组小鼠血清ALT,AST和LDH活性显著降低,肝脏中GSH含量及GSH/GSSG显著升高,并存在剂量-效应关系。病理切片显示DPPD能够明显减轻CCl4对肝组织的破坏。DPPD与同等剂量的肝炎治疗阳性药物甘草酸及甘草次酸的效果基本等同。结论:DPPD对CCl4诱导的小鼠中毒性肝炎具有明显的保护作用。
Objective : To evaluate the protective effect of 1 , 3-diphenyl-1,3-propanedione ( DPPD) on acute liver injury induced by carbon tetrachloride (CCl4) in mice. Methods: Male ICR mice were randomly ig administered with one of four DPPD dosing groups, 125, 250, 500 or 1 000 mg·kg^-1 d^-1, for 4 days. CCl4 was subcutaneously injected into the mice in 30 minutes after the 4th-day of DPPD administration. After the 24 hours of CCl4 injection, the serum ALT, AST and LDH activities were assayed. The mice were then euthanized to collect the liver tissues for the quantification of glutathione (GSH) and glutathione disulfide (GSSG) and the histopathological assessment. Results: The DPPDtreated mice showed significant reductions in the ALT, AST and LDH activities and significant increases in the GSH and GSH/GSSG levels in a dosedependent manner compared to the CCl4 alone mice. The histopathological examination found that DPPD significantly decreased the liver injury by CCl4 , and was hepatoprotectively equivalent to positive drugs glycyrrhizic acid and glycyrrhizin. Conclusion: DPPD plays an active role in the prevention of acute mice liver injury induced by CCl4.
出处
《中国新药杂志》
CAS
CSCD
北大核心
2006年第1期26-29,共4页
Chinese Journal of New Drugs
基金
国家中医药管理局项目资助(国中医药科2003LHR02号)