论文部分内容阅读
目的:探讨巴豆醛暴露致雄性大鼠神经毒性作用，分析其可能的作用机制。方法:于2019年7至10月，将24只SPF级雄性Wistar大鼠随机分为对照组和2.5、4.5、8.5 mg/kg染毒组，每组6只，分别经口给予0.0、2.5、4.5、8.5 mg/kg体重巴豆醛溶液，每周5次，连续染毒90 d。染毒结束后，测量大鼠体重，麻醉解剖取大鼠大脑组织和肝组织。测定大脑组织乙酰胆碱酯酶（AChE）活力及肝组织乙酰胆碱（ACh）水平；检测大脑组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活力以及丙二醛（MDA）和还原型谷胱甘肽（GSH）水平；酶联免疫吸附测定（ELISA）法检测大脑组织中白细胞介素6（IL-6）、白细胞介素1β（IL-1β）、肿瘤坏死因子α（TNF-α）水平。结果:与对照组比较，2.5、4.5、8.5 mg/kg染毒组大鼠大脑组织中AChE活力明显降低，8.5 mg/kg染毒组大鼠肝组织中ACh水平明显升高，差异均有统计学意义（n P<0.05）；与对照组比较，4.5、8.5 mg/kg染毒组大鼠大脑组织中MDA水平明显升高，GSH水平和SOD、GSH-Px活力明显降低，差异均有统计学意义（n P<0.05）；与对照组比较，2.5、4.5、8.5 mg/kg染毒组大鼠大脑组织中TNF-α、IL-6水平明显升高，4.5、8.5 mg/kg染毒组IL-1β水平明显升高，差异均有统计学意义（n P<0.05）。n 结论:巴豆醛暴露可致大鼠神经系统损伤，可能与氧化平衡状态改变及上调大脑组织炎性因子表达等作用有关。“,”Objective:To investigate the neurotoxicity of crotonaldehyde exposure in male rats and its possible mechanism of action.Methods:From July to October 2019, 24 specific pathogen-free male Wistar rats were randomly divided into control group and 2.5, 4.5, and 8.5 mg/kg exposure groups, with 6 rats in each group, and the rats in these groups were given oral administration of crotonaldehyde solution at doses of 0.0, 2.5, 4.5, and 8.5 mg/kg, respectively, 5 times a week for 90 consecutive days. Body weight was measured after exposure, and brain tissue and liver tissue were collected. The activity of acetylcholinesterase (AChE) in brain tissue and the level of acetylcholine (ACh) in liver tissue were measured; The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) and the levels of malondialdehyde (MDA) and reduced glutathione (GSH) in brain tissue were measured; ELISA was used to measure the levels of interleukin-6 (IL-6) , interleukin-1β (IL-1β) , and tumor necrosis factor-α (TNF-α) in brain tissue.Results:Compared with the control group, the 2.5, 4.5, and 8.5 mg/kg exposure groups had a significant reduction in the activity of AChE in brain tissue, and the 8.5 mg/kg exposure group had a significant increase in the level of ACh in liver tissue (n P<0.05) . Compared with the control group, the 4.5 and 8.5 mg/kg exposure groups had a significant increase in the level of MDA and significant reductions in the level of GSH and the activities of SOD and GSH-Px in brain tissue (n P<0.05) . Compared with the control group, the 2.5, 4.5, and 8.5 mg/kg exposure groups had significant increases in the levels of TNF-α and IL-6 in brain tissue, and the 4.5 and 8.5 mg/kg exposure groups had a significant increase in the level of IL-1β (n P<0.05) .n Conclusion:Crotonaldehyde exposure can induce nervous system injury in rats, possibly by altering oxidative balance and upregulating the expression of inflammatory factors in brain tissue.