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目的:考察1,3-二苯-1,3-丙二酮(DPPD)对N-甲基甲酰胺(NMF)急性肝损伤的保护作用。方法:小鼠经口分别灌胃给予DPPD 50,100,200 mg.kg-1,qd,连续4 d;腹腔注射给予致肝毒性剂量NMF 2 000mg.kg-1;染毒48 h后测定血清丙氨酸氨基转移酶(alanine aminotransferase,ALT)、天冬氨酸氨基转移酶(as-partate aminotransferase,AST)、乳酸脱氢酶(lactate dehydrogenase,LDH)和总胆红素(total bilirubin,T-Bil)活性;留取肝脏组织,常规石蜡包埋切片,HE染色,光镜观察肝脏组织病理变化;制备肝匀浆,测定肝组织中还原性谷胱甘肽(GSH)、氧化性谷胱甘肽(GSSG)和丙二醛(malonaldehyde,MDA)含量,计算GSH/GSSG比值。结果:与对照组比较,模型组小鼠血清ALT,AST,LDH和T-Bil水平升高,肝组织GSH/GSSG比值及MDA含量升高,肝组织细胞变性坏死;预防性给予DPPD组ALT,AST和LDH水平明显降低,肝组织GSH/GSSG比值升高,MDA含量降低,肝脏病理损伤明显改善。结论:DPPD可有效抵御NMF对ICR小鼠肝脏的毒性损伤,调动机体抗氧化应激系统为可能的机制。
Objective: To investigate the protective effect of 1,3-diphenyl-1,3-propanedione (DPPD) on acute liver injury induced by N-methyl formamide (NMF). METHODS: Mice were orally administered with DPPD 50, 100, 200 mg.kg-1, qd for 4 d after intragastric administration, respectively. Serum alanine amino groups were determined after intraperitoneal injection of NMF 2,000 mg.kg-1 Alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and total bilirubin (T-Bil) The liver tissues were collected and paraffin embedded sections were obtained. HE staining and light microscopy were used to observe the histopathological changes of liver tissues. Liver homogenates were prepared for determination of reduced glutathione (GSH), oxidized glutathione (GSSG) And malonaldehyde (MDA) content, calculated GSH / GSSG ratio. Results: Compared with the control group, the levels of serum ALT, AST, LDH and T-Bil in the model group increased, the ratios of GSH / GSSG and MDA in the liver tissue increased, and the liver cells degenerated and necrotic. AST and LDH levels were significantly reduced, liver tissue GSH / GSSG ratio increased, MDA content decreased, liver pathology improved significantly. Conclusion: DPPD can effectively resist the NMF on ICR mouse liver toxic injury, mobilize the body’s anti-oxidative stress system as a possible mechanism.