Luteolin improves nephropathy in hyperglycemic rats through anti-oxidant, anti-inflammatory, and anti-apoptotic mechanisms

Hyperglycemia can also induce the production of free radicals and the progression of inflammatory reactions. The aim of this study is to explore the potential anti-oxidant and anti-inflammatory mechanisms of luteolin in the treatment of diabetic nephropathy.Luteolin significantly reduced blood gluco...

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Bibliographic Details
Published in:Journal of Functional Foods
Main Authors: Li-You Chen, Hsin-Lin Cheng, Chih-Kai Liao, Yu-Hsiang Kuan, Tang-Jun Liang, To-Jung Tseng, Hsing-Chun Lin
Format: Article in Journal/Newspaper
Language:English
Published: Elsevier 2023
Subjects:
DML
Online Access:https://doi.org/10.1016/j.jff.2023.105461
https://doaj.org/article/287e38b7f40c471a87cb3ffcedab7b82
Description
Summary:Hyperglycemia can also induce the production of free radicals and the progression of inflammatory reactions. The aim of this study is to explore the potential anti-oxidant and anti-inflammatory mechanisms of luteolin in the treatment of diabetic nephropathy.Luteolin significantly reduced blood glucose and BUN levels in streptozotocin-induced diabetic rats and increased serum sodium and chloride levels. Histopathological staining of the kidney showed that luteolin effectively inhibits glycoprotein deposition and production of collagen fibers in the kidney. On Western blotting, luteolin increased anti-oxidant enzymes in the kidney by up-regulating NF-E2-related factor 2 (Nrf2). In DML rats, the expression of inflammatory cytokines decreased significantly with down-regulation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB). In addition, luteolin inhibited the activation of phosphoinositide 3-kinase/protein kinase B (PI3K/Akt) signaling pathway and the expressions of its downstream apoptosis-related proteins.In conclusion, luteolin slows the progression of nephropathy through anti-hyperglycemic, anti-inflammatory, anti-oxidant, and anti-apoptotic mechanisms.