癌变·畸变·突变2017，Vol.29Issue(4)：251-255,5.DOI:10.3969/j.issn.1004-616x.2017.04.002
阿特拉津对青春期大鼠黑质区多巴胺能神经元的损伤作用
Induction of dopaminergic neuron degeneration by atrazine in substantia nigra in adolescent rats
摘要
Abstract
OBJECTIVE:To study effects of atrazine (ATR) on neuronal degeneration in adolescent rats. METHODS:4 weeks old Wistar male rats were randomly subdivided into 4 groups: control and ATR test groups. All rats were treated with ATR: 50,100 and 200 mg/kg body weight per day (five times per week) for 45 days by oral gavage. They were sacrificed at 12 h after the last ATR injection. The entire midbrain was collected and stored frozen at -80℃. The presence of tyrosine hydroxylase(TH) was detected by immunohistochemistry SP in dopaminergic neurons. TH expression in mRMA and protein was measured using real-time PCR and Western blot.RESULTS:Immunohistochemical results showed that,compared with the control group,the number of TH positive cells in the 200 mg/kg ATR group was significantly decreased (P<0.01). In addition,qPCR results show that expression of TH mRNA and Bcl-2 mRNA was significantly decreased in the 100 and 200 mg/kg ATR groups,and expression of p53 mRNA and Caspase-9 mRNA was significantly increased in the 200 mg/kg ATR group,the difference was statistically significant (P<0.05). Western blot results show that expression of TH and Bcl-2 protein was significantly decreased in the 100 and 200 mg/kg ATR groups compared with the control group. Expression of p53 protein in the ATR group was significantly increased at 100 and 200 mg/kg,and Caspase-9 protein in he 200 mg/kg ATR group was significantly increased,the difference was statistically significant (P<0.05).CONCLUSION:Atrazine caused damage to the dopaminergic neurons in the substantia nigra of rats and activated the apoptotic pathway which led to the dopaminergic neuronal death.关键词
阿特拉津/多巴胺能神经元/免疫组织化学/酪氨酸脱氢酶Key words
atrazine/dopaminergic neurons/immunohistochemistry/tyrosine hydroxylase分类
医药卫生引用本文复制引用
马焜,吴昊宇,李鹏,王丽,李百祥..阿特拉津对青春期大鼠黑质区多巴胺能神经元的损伤作用[J].癌变·畸变·突变,2017,29(4):251-255,5.基金项目
国家自然科学基金资助项目(81273109) （81273109）
