Polysaccharide from Cordyceps cicadae inhibit mitochondrial apoptosis to ameliorate drug-induced kidney injury via Bax/Bcl-2/Caspase-3 pathway

Polysaccharide from Cordyceps cicadae protects against GM-induced DIKI by alleviating renal tubular epithelial cell apoptosis. [Display omitted] •CCPa could alleviate gentamicin induced HK-2 cell death.•CCPa could reverse gentamicin induced mice kidney injury.•The role of CCPa in kidney protection i...

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Published inJournal of functional foods Vol. 97; p. 105244
Main Authors Zhu, Lijun, Yu, Tian, Yang, Li, Liu, Tao, Song, Zhuoyue, Liu, Shihui, Zhang, Danyan, Tang, Chunzhi
Format Journal Article
LanguageEnglish
Published Elsevier Ltd 01.10.2022
Elsevier
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Summary:Polysaccharide from Cordyceps cicadae protects against GM-induced DIKI by alleviating renal tubular epithelial cell apoptosis. [Display omitted] •CCPa could alleviate gentamicin induced HK-2 cell death.•CCPa could reverse gentamicin induced mice kidney injury.•The role of CCPa in kidney protection is to regulate the Bax/Bcl-2/Caspase-3 pathway. Drug-induced kidney injury (DIKI) refers to kidney damage caused by nephrotoxic drugs. Unfortunately, there are no effective prevention measures. Here, the protective effect of polysaccharide from Cordyceps cicadae (CCPa) on DIKI was evaluated. The results of in vivo experiment showed that the kidney injury induced by gentamicin (GM) was significantly improved after CCPa intervention. For instance, CCPa could ameliorate renal function (the levels of SCr and BUN) and renal pathological damage, inhibit the inflammatory factors (IL-6 and TNF-α) and reduce the amount of apoptotic cells in the kidney. Furthermore, both in vivo and in vitro experiments showed that CCPa dose-dependently inhibited mitochondrial apoptosis and regulated the expression of Bax/Bcl-2/caspase-3 pathway-related proteins, thus playing a protective role in kidney. The results provided a basis for the prevention of CCPa on DIKI and CCPa could be developed as a healthy food or drug for kidney protection.
ISSN:1756-4646
2214-9414
DOI:10.1016/j.jff.2022.105244