Renoprotective Effect of Pediococcus acidilactici GKA4 on Cisplatin-Induced Acute Kidney Injury by Mitigating Inflammation and Oxidative Stress and Regulating the MAPK, AMPK/SIRT1/NF-κB, and PI3K/AKT Pathways

Chia Nan University of Pharmacy & Science Institutional Repository > 行政單位 > 123 > Item 310902800/34664

jsp.display-item.identifier=請使用永久網址來引用或連結此文件: https://ir.cnu.edu.tw/handle/310902800/34664

標題:	Renoprotective Effect of Pediococcus acidilactici GKA4 on Cisplatin-Induced Acute Kidney Injury by Mitigating Inflammation and Oxidative Stress and Regulating the MAPK, AMPK/SIRT1/NF-κB, and PI3K/AKT Pathways
作者:	Lin, Wen-Hsin Jiang, Wen-Ping Chen, Chin-Chu Lee, Li-Ya Tsai, You-Shan Chien, Liang-Hsuan Chou, Ya-Ni Deng, Jeng-Shyan Huang, Guan-Jhong
貢獻者:	China Medical University Taiwan Chia Nan University of Pharmacy & Science Grape King Bio Ltd China Medical University Taiwan Asia University Taiwan
關鍵字:	mechanisms nephrotoxicity
日期:	2022
上傳時間:	2023-12-11 14:03:49 (UTC+8)
出版者:	MDPI
摘要:	Acute kidney injury (AKI) describes a sudden loss of kidney function and is associated with a high mortality. Pediococcus acidilactici is a potent producer of bacteriocin and inhibits the growth of pathogens during fermentation and food storage; it has been used in the food industry for many years. In this study, the potential of P. acidilactici GKA4 (GKA4) to ameliorate AKI was investigated using a cisplatin-induced animal model. First, mice were given oral GKA4 for ten days and intraperitoneally injected with cisplatin on the seventh day to create an AKI mode. GKA4 attenuated renal histopathological alterations, serum biomarkers, the levels of inflammatory mediators, and lipid oxidation in cisplatin-induced nephrotoxicity. Moreover, GKA4 significantly decreased the expression of inflammation-related proteins and mitogen-activated protein kinase (MAPK) in kidney tissues. Eventually, GKA4 also increased the levels of related antioxidant enzymes and pathways. Consistently, sirtuin 1 (SIRT1) upregulated the level of autophagy-related proteins (LC3B, p62, and Beclin1). Further studies are needed to check our results and advance our knowledge of the mechanism whereby PI3K inhibition (wortmannin) reverses the effect of GKA4 on cisplatin-treated AKI. Taken together, GKA4 provides a therapeutic target with promising clinical potential after cisplatin treatment by reducing oxidative stress and inflammation via the MAPK, AMP-activated protein kinase (AMPK)/SIRT1/nuclear factor kappa B (NF-kappa B), and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) axes.
關聯:	NUTRIENTS, v.14, n.CB2, pp.CC2, pp.-2743,
显示于类别:	[行政單位] 123

文件中的档案:

档案	描述	大小	格式	浏览次数
index.html		0Kb	HTML	113	检视/开启

在CNU IR中所有的数据项都受到原著作权保护.

TAIR相关文章

数据加载中.....