Archives of physiology and biochemistry · 2025
Menthol ameliorates thioacetamide-induced renal fibrosis in rats by upregulating SIRT1/Nrf2 and downregulating TGF-β1/Smad3 signalling pathways.
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Babaei Elaheh, Asle-Rousta Masoumeh, Mahmazi Sanaz
Аннотация
INTRODUCTION: Renal fibrosis is a significant factor in the progression of chronic kidney disease. This study examined how menthol affects thioacetamide (TA)-induced biochemical, molecular, and histopathological damage that leads to renal fibrosis and dysfunction.
METHODS: Male Wistar rats were treated with TA (200 mg/kg, intraperitoneally) twice a week for four consecutive weeks, along with menthol (10 mg/kg, intraperitoneally) for the same duration.
RESULTS: Menthol effectively reduced oxidative stress and inflammation in the kidneys of rats treated with TA. It also lowered the expression of TGF-β1, SMAD3, α-SMA, and KIM-1. Furthermore, menthol prevented the decline in SIRT1 mRNA expression and protein levels while increasing the expression of Nrf2. It inhibited collagen deposition and histological damage in the kidneys and prevented the rise in serum creatinine and BUN levels.
CONCLUSION: Menthol provides protective effects against renal fibrosis induced by thioacetamide. Its antifibrotic effects are mediated by upregulating SIRT1/Nrf2 and downregulating TGF-β1/Smad3 pathways.
METHODS: Male Wistar rats were treated with TA (200 mg/kg, intraperitoneally) twice a week for four consecutive weeks, along with menthol (10 mg/kg, intraperitoneally) for the same duration.
RESULTS: Menthol effectively reduced oxidative stress and inflammation in the kidneys of rats treated with TA. It also lowered the expression of TGF-β1, SMAD3, α-SMA, and KIM-1. Furthermore, menthol prevented the decline in SIRT1 mRNA expression and protein levels while increasing the expression of Nrf2. It inhibited collagen deposition and histological damage in the kidneys and prevented the rise in serum creatinine and BUN levels.
CONCLUSION: Menthol provides protective effects against renal fibrosis induced by thioacetamide. Its antifibrotic effects are mediated by upregulating SIRT1/Nrf2 and downregulating TGF-β1/Smad3 pathways.