摘要
目的 探讨大剂量VitC对丙烯酰胺 (ACR)诱导小鼠脑损伤的保护作用。方法 连续小鼠腹腔注射不同剂量ACR(2 5mg/kg·d)为染毒组 ,VitC组在小鼠染毒的同时腹腔注射VitC(5 0mg/kg·d) ,正常对照组以等量生理盐水注射。在用药第 5天、10天分离小脑采用硫巴比妥酸法 (TBA)测定过氧化脂质 (LPO)的含量 ,采用逆转录 聚合酶链反应检测鼠纤粘连蛋白 (fibronectin ,Fn)基因的表达。结果 ACR组小脑LPO与正常对照组比较均有显著差异 (P <0 .0 5 ) ;且低剂量ACR组 (第 5天、10天 )之间 ,VitC组与ACR组比较均有显著性差异 (P <0 .0 5 )。ACR组Fn基因表达明显上调 ,VitC组Fn表达下降。结论 ACR神经毒性与氧自由基增多密切相关 ,VitC能够减轻ACR神经毒作用。ACR对Fn基因表达的影响 ,可能介导其神经毒作用。
Objective To study the protection of Vitamin C from acrylamide (ACR)-mediated neurotoxicity of mice.Methods The mice were treated by peritoneal injection of ACR with a dose of 25 mg/kg·d as ACR group.The mice were treated with same dosage of ACR and Vit C (每日50 mg/kg) as Vit C group while the normal control were treated with normal saline.These mice were decapitated to isolate the cerebellum and cerebral cortex of mice on 5 day and 10 day.The method of thiobarbituric acid positive(TBA)was used to assay the content of LPO.Results transcribed polymerase chain reaction was carried out to detect the expression of gene fibronectin(Fn) in cerebellum.Results These results showed that there was significant difference between ACR group and control group (P<0.05). The content of LPO in Vit C group showed significant difference as compared to ACR group (P<0.05). The gene of Fn in ACR group showed higher expression than that in control and Vit C group.Conclusion These data suggest that the neurotoxicity of ACR may directly relate to the higher level of oxidative free radicals,and Vit C can reduce the ACR-mediated neurotoxicity.The effects of ACR on the gene expression of Fn in cerebellum may play an important role in pathology of central nerve system.
出处
《同济大学学报(医学版)》
CAS
2004年第5期372-373,377,共3页
Journal of Tongji University(Medical Science)