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    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
    Department of Pharmacy, 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.14, 2877
    顯示於類別:[藥學系(所)] 期刊論文

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