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. 2019 Mar 28;24(7):1214.
doi: 10.3390/molecules24071214.

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

Rosa Martha Pérez Gutierrez  1 , Abraham Heriberto García Campoy  2 , Silvia Patricia Paredes Carrera  3 , Alethia Muñiz Ramirez  4 , José Maria Mota Flores  5 , Sergio Odin Flores Valle  6
Affiliations

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

Rosa Martha Pérez Gutierrez et al. Molecules. .

Abstract

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.

Keywords: Eysenhardtia polystachya; advanced glycation end-product; diabetic mice; dihydrochalcone; renoprotective.

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Conflict of interest statement

The authors claim no conflict of interest in this study.

Figures

Figure 1
Figure 1
(A) Dihydrochalcone 1 isolated from bark of Eysenhardtia polystachya; (B) Heteronuclear Multiple Bond Connectivity (HMBC) of 1.
Figure 2
Figure 2
(A) examination of urine volume at the fifth weeks; (B) examination of food consumptions at the fifth weeks; (C) examination of water intake at the fifth weeks; (D) examination of body weigh at the fifth weeks; Results are expressed as mean ± SD; a p < 0.05 vs. diabetic control.
Figure 3
Figure 3
(A) Images of kidney representative of five weeks of the different treatments; (B) examination of kidney weight at the fifth weeks; Results are expressed as mean ± SD; a p < 0.05 vs. diabetic control.
Figure 4
Figure 4
Examination of inflammation markers ICAM-1 in glomeruli of kidneys from diabetic mice at the fifth weeks; Results are expressed as mean ± SD; a p < 0.05 vs. diabetic control.
Figure 5
Figure 5
(A) Circulating AGE levels measured as absolute fluorescence at 5 weeks of experimental period; (B) Circulating AGE levels expressed as advanced glycation index. Results are expressed as mean ± SD; a p < 0.05 vs. diabetic control.
Figure 6
Figure 6
Kidney sections from mice by light microscopy (H and E stained). (A) Control group, (B) Diabetic control, (C) D + 1 (25 mg/kg), (D) D + 1 (50 mg/kg), (E) D + 1 (100 mg/kg), (F) D + MET (200 mg/kg).
See this image and copyright information in PMC

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