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Kaempferol attenuates spinal cord injury by interfering inflammatory and oxidative stress by targeting the p53 protein: a molecular docking analysis

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Abstract

Background

Kaempferol (KMF) is a flavone reported to have anti-oxidant and anti-inflammatory activity.

Objective

The present study screened the effect of KMF in the animal model of spinal cord injury (SCI).

Results

KMF caused a significant inhibition of spinal cord injury mediated oxidative stress and also suppressed the inflammatory reactions. The treatment of KMF also inhibited the levels of p53, TGF-β1 and COX-2 whereas a significant elevation in Bcl-2/Bax ratio was observed after the rats were treated with KMF. The in silico docking analysis suggested potential binding of KMF having lower energy with p53 confirming the potential target of KMF.

Conclusion

The treatment of KMF exerted neuroprotective effect by improving the anti-oxidant status and inflammatory response. The significant spinal cord injury protective effect of KMF in rats was attributed by targeting p53 and Bcl-2/Bax ratio.

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Acknowledgement

The authors very much thankful to the staff and management of The Second Affiliated Hospital of Nanchang University.

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Authors

Contributions

All the authors contributed equally in preparing the manuscript. LC and KC planned the study. YG, CL, WM, WZ, JZ, HZ along with LC and KC performed the experiments and formatted the data. All the authors contributed to preparing the manuscript and reviewed the paper before submitting.

Corresponding author

Correspondence to Kai Cao.

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Conflict of interest

Lu Chen, Kai Cao, Yurong Gu, Chao Luo, Wei Mao, Weijun Zhou, Jinwei Zhu, Huying Zhang authors have no conflict of interest.

Ethical approval

The animal studies were approved by the ethical review board of The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China, the approval number for the study was S0144C.

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Chen, L., Cao, K., Gu, Y. et al. Kaempferol attenuates spinal cord injury by interfering inflammatory and oxidative stress by targeting the p53 protein: a molecular docking analysis. Mol. Cell. Toxicol. 17, 257–266 (2021). https://doi.org/10.1007/s13273-021-00132-x

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