3′-O-β-d-glucopyranosyl-α,4,2′,4′,6′-pentahydroxy-dihydrochalcone, from Bark of Eysenhardtia polystachya Prevents Diabetic Nephropathy via Inhibiting Protein Glycation in STZ-Nicotinamide Induced Diabetic Mice
Natural Products Research Laboratory, Higher School of Chemical Engineering and Extractive Industries, National Polytechnic Institute, Av. Instituto Politécnico Nacional S/N, Unidad Profesional Adolfo Lopez Mateos, Ciudad de México CP 07708, Mexico
Sustainable Nanomaterials Laboratory, Higher School of Chemical Engineering and Extractive Industries, National Polytechnic Institute (IPN) Professional Unit Adolfo Lopez Mateos, S/N Av. Instituto Politécnico Nacional, Ciudad de México CP 07708, Mexico
CONACYT/IPICYT-CIIDZA, Camino a la Presa de San José 2055, Col. Lomas 4 Sección, San Luis Potosí CP 78216, Mexico
Green Chemistry Research Laboratory, School of Chemical Engineering and Extractive Industries, National Polytechnic Institute, Av. Instituto Politécnico Nacional S/N, Unidad Profesional Adolfo Lopez Mateos, Ciudad de México CP 07708, Mexico
Author to whom correspondence should be addressed.
Academic Editor: Raffaele Capasso
Molecules 2019, 24(7), 1214; https://doi.org/10.3390/molecules24071214
Received: 5 February 2019 / Revised: 20 March 2019 / Accepted: 22 March 2019 / Published: 28 March 2019
(This article belongs to the Special Issue Plant Extracts: Biological and Pharmacological Activity)
Previous studies have shown that accumulation of advanced glycation end products (AGEs) can be the cause of diabetic nephropathy (DN) in diabetic patients. Dihydrochalcone 3′-O-β-d-glucopyranosyl α,4,2′,4′,6′-pentahydroxy–dihydrochalcone (1) is a powerful antiglycation compound previously isolated from Eysenhardtia polystachya. The aim was to investigate whether (1) was able to protect against diabetic nephropathy in streptozotocin (STZ)-induced diabetic mice, which displayed renal dysfunction markers such as body weight, creatinine, uric acid, serum urea, total urinary protein, and urea nitrogen in the blood (BUN). In addition, pathological changes were evaluated including glycated hemoglobin (HbA1c), advanced glycation end products (AGEs) in the kidney, as well as in circulation level and pro-inflammatory markers ICAM-1 levels in diabetic mice. After 5 weeks, these elevated markers of dihydrochalcone treatment (25, 50 and 100 mg/kg) were significantly (p < 0.05) attenuated. In addition, they ameliorate the indices of renal inflammation as indicated by ICAM-1 markers. The kidney and circulatory AGEs levels in diabetic mice were significantly (p < 0.05) attenuated by (1) treatment. Histological analysis of kidney tissues showed an important recovery in its structure compared with the diabetic group. It was found that the compound (1) attenuated the renal damage in diabetic mice by inhibiting AGEs formation.