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The Protective Effect of Baicalin Against Lead-Induced Renal Oxidative Damage in Mice

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Abstract

Lead (Pb) exposure is a global environmental problem that can deplete body antioxidant enzymes, causing damage to various macromolecules and ultimately cell death. Pb exposure could lead to serious renal damage. Baicalin, a traditional Chinese medicine, could protect against renal injury through inhibition of oxidative stress and apoptosis. This study was designed to investigate the protective efficacy of baicalin against Pb-induced nephrotoxicity in mice and to elucidate the potential mechanisms using animal experiment. The results revealed that baicalin decreased Pb-induced bodyweight loss, declined kidney coefficients, and ameliorated renal function and structure in a dose-dependent manner. Meanwhile, baicalin dose dependently increased Pb-induced activity of SOD and GSH-Px, while the content of MDA in the kidney was decreased. In addition, baicalin enhanced the Bcl-2/Bax ratio associated with apoptosis in the kidney. These data indicated that further investigation of the use of baicalin as a new natural chemopreventive agent against Pd poisoning is warranted.

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Acknowledgments

This work was supported by a grant from the National Natural Science Foundation of China (Nos. 31272622 and 31472248) and Jilin Province Science Foundation for Youths (No. 20130522087JH).

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Correspondence to Yongguo Cao or Naisheng Zhang.

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All of the animal studies were conducted in accordance with the experimental practices and standards that were approved by the Animal Welfare and Research Ethics Committee at Jilin University under the approved protocol number JLUA-1309. The protocols were reviewed and approved by the committee. All of the animal studies were performed under isoflurane anesthesia.

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The authors declare that they have no competing interests.

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Zhang, Z., Gao, X., Guo, M. et al. The Protective Effect of Baicalin Against Lead-Induced Renal Oxidative Damage in Mice. Biol Trace Elem Res 175, 129–135 (2017). https://doi.org/10.1007/s12011-016-0731-2

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