Resveratrol prevents diabetic nephropathy by reducing chronic inflammation and improving the blood glucose memory effect in non-obese diabetic mice

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Abstract

Chronic inflammation plays an important role in the development of diabetic nephropathy. Advanced glycation end product receptor (RAGE), nuclear factor kappa B (NF-κB) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase 4 (NOX4) are involved in the development of inflammation. Resveratrol is a plant antitoxin; it is believed to have anti-inflammatory effects and can improve blood glucose. We speculate that resveratrol treatment can protect renal function by reducing blood glucose, decreasing the expression of inflammatory factors. Non-obese diabetic (NOD) mice were randomly divided into three groups: T1DM, insulin (INS) and resveratrol (Res) groups. Mice without diabetes were classified as the non-diabetic control group (NOD-C group). The blood glucose (BG) level, blood urea nitrogen (BUN) level, serum creatinine (SCr) level and 24-h urinary microalbumin quantitative (UMA) were measured. The glomerulosclerosis index and basement membrane thickness were calculated under light and electron microscopes. The expression levels of RAGE, NF-кB (P65) and NOX4 in renal tissues were detected by Western blot analysis. We found that resveratrol treatment significantly reduced blood glucose within 28 days of the experiment, but the hypoglycemic effect was not lasting. At the same time, resveratrol reduced BUN, SCr, 24 h UMA and the expression of the inflammatory factors RAGE, NF-кB (P65) and NOX4 and improved the renal pathological structure. We believe that resveratrol improves renal function not only by its anti-inflammatory effect but also by improving the metabolic memory of hyperglycemia.

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Xian, Y., Gao, Y., Lv, W., Ma, X., Hu, J., Chi, J., … Wang, Y. (2020). Resveratrol prevents diabetic nephropathy by reducing chronic inflammation and improving the blood glucose memory effect in non-obese diabetic mice. Naunyn-Schmiedeberg’s Archives of Pharmacology, 393(10), 2009–2017. https://doi.org/10.1007/s00210-019-01777-1

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