Zhou Lihua, Zhang Xun, Yu Yingying, Zhang Panpan
School of Public Health, Bengbu Medical University, Bengbu 233030, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2025 May 20;45(5):893-900. doi: 10.12122/j.issn.1673-4254.2025.05.01.
To explore whether the antioxidant axis Nrf2/HO-1 is involved in the regulation of hippocampus injury induced by cypermethrin and its underlying mechanism.
Ten-week-old C57BL/6 mice were randomly divided into control group and cypermethrin exposure groups with low, medium, and high exposure levels. After 21 days of oral gavage of corn oil (control) or cypermethrin, the levels of MDA, T-SOD, GSH-Px and CAT in the hippocampus of the mice were examined to evaluate the oxidative stress levels. HE staining was used to observe morphological changes of the hippocampal neurons. Western blotting, immunofluorescence staining and RT-qPCR were employed to detect the protein expressions and mRNA expression of Nrf2 and HO-1 and HO-1.
Subacute oral exposure to cypermethrin significantly increased MDA level, decreased the activities of antioxidant enzymes T-SOD, GSH-Px and CAT, and induced neuronal damage in the CA1 and CA3 regions in the hippocampus of C57BL/6 mice. Cypermethrin exposure also caused Nrf2 protein translocation from the cytoplasm to the nucleus, accompanied by upregulated expression levels of the key antioxidant factor Nrf2 and its downstream target kinase HO-1.
Cypermethrin exposure dose-dependently causes oxidative damage in the hippocampus of C57BL/6 mice, which is regulated by the Nrf2/HO-1 antioxidant pathway.
探讨抗氧化轴Nrf2/HO-1是否参与氯氰菊酯诱导的海马损伤调控及其潜在机制。
将10周龄C57BL/6小鼠随机分为对照组和低、中、高暴露剂量的氯氰菊酯暴露组。经口灌胃玉米油（对照组）或氯氰菊酯21天后，检测小鼠海马中丙二醛（MDA）、总超氧化物歧化酶（T-SOD）、谷胱甘肽过氧化物酶（GSH-Px）和过氧化氢酶（CAT）水平，以评估氧化应激水平。采用苏木精-伊红（HE）染色观察海马神经元形态变化。运用蛋白质印迹法、免疫荧光染色和实时定量聚合酶链反应（RT-qPCR）检测Nrf2和HO-1的蛋白质表达及mRNA表达。
亚急性经口暴露于氯氰菊酯显著升高了C57BL/6小鼠海马中MDA水平，降低了抗氧化酶T-SOD、GSH-Px和CAT的活性，并诱导海马CA1和CA3区神经元损伤。氯氰菊酯暴露还导致Nrf2蛋白从细胞质转位至细胞核，同时关键抗氧化因子Nrf2及其下游靶激酶HO-1的表达水平上调。
氯氰菊酯暴露剂量依赖性地导致C57BL/6小鼠海马氧化损伤，该损伤受Nrf2/HO-1抗氧化途径调控。
