Renal Protective Effects of Sparstolonin B in a Mouse Model of Sepsis

• Published in: Biotechnology and bioprocess engineering Vol. 27; no. 2; pp. 157 - 162
• Main Authors: Kim, Chaeyeong, Ryu, Soo Ho, Kim, Nayeon, Lee, Wonhwa, Bae, Jong-Sup
• Format: Journal Article
• Language: English
• Published: Seoul The Korean Society for Biotechnology and Bioengineering 01.04.2022; Springer Nature B.V; 한국생물공학회
• Subjects: antioxidant activity; Antioxidants; bioprocessing; Biotechnology; blood serum; Catalase; Cecum; Chemistry; Chemistry and Materials Science; Creatinine; Damage; death; Glutathione; Glutathione peroxidase; Industrial and Production Engineering; Inflammation; Interleukin 6; Kidneys; Lethality; Lipid peroxidation; Lipids; mice; necrosis; neoplasms; NF-κB protein; Nitric acid; Nitric oxide; Nitric-oxide synthase; Oxidation; Peroxidase; Peroxidation; Plasma levels; Research Paper; Scirpus; Sepsis; Sparganium eurycarpum; Superoxide dismutase; transcription factor NF-kappa B; Tubers; Tumor necrosis factor-α; Urea; urea nitrogen; urine; 생물공학; antioxidant; renal toxicity; sparstolonin B; sepsis; renal injury
• ISSN: 1226-8372; 1976-3816
• DOI: 10.1007/s12257-021-0319-3

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.