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Overexpression of Cpg15 Alleviates the Oxidative Stress in Neuronal Cells Via Regulating Redox Enzymes and Nrf2 Antioxidative Pathway

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Abstract

Oxidative stress is becoming increasingly implicated in the development of a variety of neurological disorders. However, the underlying mechanism remains elusive. In the present study, we investigated the function and related signal pathway which Cpg15, a neuronal-specific expressed neurotrophic factor, plays in the oxidative stress of neurons using a H2O2-treated N2a cell model. The results showed that the Cpg15 expression was decreased under oxidative stress, and overexpression of Cpg15 increased the activity of antioxidative SOD enzymes and decreased the expression level of prooxidative COX2 enzyme, and the level of oxidative products malondialdehyde (MDA), indicating its function and potential mechanism in alleviating the oxidative stress of cells. The results also indicated that the Nrf2/HO-1 antioxidative pathway was involved in the Cpg15-mediated alleviation of oxidative stress. Also, overexpression of Cpg15 activated the Nrf2 antioxidative pathway in the thalamus of the REM sleep-deprived mice. In conclusion, our results implied that supplemental expression of Cpg15 may alleviate oxidative stress in neuronal cells via regulating the redox enzymes or activating the Nrf2 antioxidant pathway.

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Acknowledgments

This work was supported by grants from the National Foundation of Natural Sciences of China (grant numbers 31771112, 31571037), Shanghai Municipal Science and Technology Major Project (No.2018SHZDZX01), ZJ Lab, and Shanghai Center for Brain Science and Brain-Inspired Technology.

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Correspondence to **an-Hua Chen.

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Yi Jiang, Jun-Jie Li and Ya-Wei Mu are contributed equally to this work.

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Jiang, Y., Li, JJ., Mu, YW. et al. Overexpression of Cpg15 Alleviates the Oxidative Stress in Neuronal Cells Via Regulating Redox Enzymes and Nrf2 Antioxidative Pathway. Neurotox Res 40, 365–372 (2022). https://doi.org/10.1007/s12640-022-00473-y

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