Biotechnology and Bioprocess Engineering 2022; 27(2): 157-162  
Renal Protective Effects of Sparstolonin B in a Mouse Model of Sepsis
Chaeyeong Kim, Soo Ho Ryu, Nayeon Kim, Wonhwa Lee, and Jong-Sup Bae
Chaeyeong Kim, Soo Ho Ryu, Nayeon Kim, Jong-Sup Bae*
College of Pharmacy, Research Institute of Pharmaceutical Sciences, Kyungpook National University, Daegu 41566, Korea
Tel: +82-53-950-8570; Fax: +82-53-950-8557
E-mail: baejs@knu.ac.kr
Wonhwa Lee*
Department of Chemistry, Sungkyunkwan University, Suwon 16419, Korea
Tel: +82-31-290-5393; Fax: +82-31-290-7075
E-mail: Wonhwalee@skku.edu
These authors contributed equally to this work.
Received: October 20, 2021; Revised: October 31, 2021; Accepted: October 31, 2021; Published online: April 30, 2022.
© The Korean Society for Biotechnology and Bioengineering. All rights reserved.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract
Sparstolonin B (SsnB) exists in the tubers of Scirpus yagara and Sparganium stoloniferum, and it is known to modulate inflammatory mediators. Here, we investigated whether SsnB could reduce the renal functional damage in a cecal ligation and puncture (CLP)-induced septic mice. The effect of SsnB was measured via assessment of blood urea nitrogen (BUN), serum creatinine, total glutathione, lipid peroxidation, catalase activity, glutathione peroxidase activity, and superoxide dismutase activity. Our findings showed that SsnB treatment in mice with CLP-induced renal damage elevated the BUN and creatinine levels in plasma and protein levels in the urine. In contrast, the excessive production of nitric acid and induction of nitric oxide synthase were decreased. Moreover, SsnB inhibited the activation of nuclear factor-kappa B, reduced the plasma levels of tumor necrosis factor-α and interleukin-6, and thus reduced lethality. SsnB also increased lipid peroxidation and restored the levels of superoxide dismutase, glutathione peroxidase, and catalase in kidney tissues, thereby enhancing the antioxidant defense system. Conclusively, our results indicate that SsnB can protect mice from sepsis-induced renal injury.
Keywords: sparstolonin B, sepsis, antioxidant, renal injury, renal toxicity


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