Abstract
Renal inflammation can result in renal injury. Uric acid (UA) is the final product of purine metabolism in humans and because of the lack of urate oxidase, UA may accumulate in tissues, including kidney, causing inflammation. Galangin was isolated from a traditional Chinese medicine plant and possesses several beneficial effects, working as an anti-oxidant, anti-mutagenic, anti-tumor, anti-inflammatory, anti-microbial, and anti-viral agent. Therefore, this study aimed at investigating the molecular mechanism of galangin in the attenuation of UA induced renal inflammation in normal rat kidney epithelial cells NRK-52E. Our findings suggested that galangin treatment efficiently protected NRK-52E cells against UA induced renal inflammation by decreasing tumor necrosis factor (TNF)-α, interleukin (IL)-1β, IL-18, prostaglandin E2 (PGE2), and nitric oxide (NO) release, and it inhibited nitric oxide synthase (iNOS), prostaglandin endoperoxide synthase 2 (PTGS2), TNF-α, IL-1β, and IL-18 mRNA expression. In addition, galangin was not exerting any cytotoxicity at the concentrations that were effective against inflammation as assessed by CCK8 assay. Moreover, western blotting showed that galangin treatment effectively inhibited nuclear factor-kappa B (NF-κB), phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) and nucleotide-binding domain- (NOD-) like receptor protein 3 (NLRP3) signaling pathway activation. Taken together, these findings suggested that galangin plays a pivotal role in renal inflammation by suppressing inflammatory responses, which might be closely associated with the inhibition of NLRP3 inflammasome, NF-κB and PI3K/AKT signaling pathway activation.
Highlights
Renal inflammation, which is characterized by the infiltration of inflammatory cells into the renal parenchyma, is an imperative pathologic process in the evolution of renal injury [1]
The results showed that galangin did not affect normal cells growth at concentrations up to 20 μg/ml compared to the control group
The results showed that the mRNA expression of inhibited nitric oxide synthase (iNOS), prostaglandin endoperoxide synthase 2 (PTGS2), tumor necrosis factor (TNF)-α, IL-1β and IL-18 was significantly increased in uric acid (UA) treated NRK-52E cells compared to their expression in the control group (p
Summary
Renal inflammation, which is characterized by the infiltration of inflammatory cells into the renal parenchyma, is an imperative pathologic process in the evolution of renal injury [1]. A growing number of epidemiologic and experimental evidences suggest that several endogenous substances, especially uric acid (UA), the final product of purine metabolism in humans and higher primates[2], play an important role in mediating inflammation stimulated by a pathologic insult and tissue damage. Exposure of NRK-52E cells to UA induces inflammation that is characterized by the overproduction of pro-inflammatory cytokines and mediators. Increasing evidence shows that various proinflammatory cytokines and mediators, including TNF-α, IL1β, IL-18, NO, and PGE2, are involved in UA induced renal inflammation, chronic kidney disease, and even renal failure [7,8,9]. The suppression of the inflammatory response might be a potential prevention of the development of renal inflammation
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