Zhang S M, Zhang Z H, Zhang B, Zhang Q
Shandong Academy of Occupational Health and Occupational Medicine, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan 250062, China.
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2021 Jan 20;39(1):1-4. doi: 10.3760/cma.j.cn121094-20200106-00015.
To investigate the neurotoxicity of crotonaldehyde exposure in male rats and its possible mechanism of action. 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. 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 (<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 (<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 (<0.05) . Crotonaldehyde exposure can induce nervous system injury in rats, possibly by altering oxidative balance and upregulating the expression of inflammatory factors in brain tissue.
研究巴豆醛暴露对雄性大鼠的神经毒性及其可能的作用机制。2019年7月至10月，将24只无特定病原体雄性Wistar大鼠随机分为对照组和2.5、4.5、8.5mg/kg暴露组，每组6只，分别给予各组大鼠口服0.0、2.5、4.5、8.5mg/kg剂量的巴豆醛溶液，每周5次，连续90天。暴露后测量体重，并采集脑组织和肝组织。检测脑组织中乙酰胆碱酯酶（AChE）活性和肝组织中乙酰胆碱（ACh）水平；检测脑组织中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH-Px）活性以及丙二醛（MDA）、还原型谷胱甘肽（GSH）水平；采用酶联免疫吸附测定（ELISA）法检测脑组织中白细胞介素-6（IL-6）、白细胞介素-1β（IL-1β）和肿瘤坏死因子-α（TNF-α）水平。与对照组相比，2.5、4.5、8.5mg/kg暴露组脑组织中AChE活性显著降低，8.5mg/kg暴露组肝组织中ACh水平显著升高（P<0.05）。与对照组相比，4.5、8.5mg/kg暴露组脑组织中MDA水平显著升高，GSH水平、SOD和GSH-Px活性显著降低（P<0.05）。与对照组相比，2.5、4.5、8.5mg/kg暴露组脑组织中TNF-α和IL-6水平显著升高，4.5、8.5mg/kg暴露组IL-1β水平显著升高（P<0.05）。巴豆醛暴露可诱导大鼠神经系统损伤，可能是通过改变氧化平衡和上调脑组织中炎症因子的表达来实现的。
