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

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.

<p>Apigenin-Loaded Solid Lipid Nanoparticle Attenuates Diabetic Nephropathy Induced by Streptozotocin Nicotinamide Through Nrf2/HO-1/NF-kB Signalling Pathway</p>

“…This could ultimately result in damage and toxicity. 27 The fact that oxidative stress is the major factor for DM-related complications including DN is acknowledged widely. 28,29 The membrane fatty acid (polyunsaturated) is degraded by ROS and leads to production of 4-HNE and MDA, which is an unstable aldehyde that could form a covalent protein adduct which is a trait of oxidative stress in tissue injuries.…”

Triptolide protects against podocyte injury in diabetic nephropathy by activating the Nrf2/HO-1 pathway and inhibiting the NLRP3 inflammasome pathway

“…Accumulated ROS may interact with fatty acids (polyunsaturated), leading to the formation of lipid peroxidation in renal tissues, which may ultimately lead to damage and toxicity [ 62 ]. On the other hand, OS is widely acknowledged as a major factor in DM-related complications, including DN [ 63 , 64 ], while TP is widely known for its good antioxidant effects [ 65 , 66 ].…”

A Nucleoside/Nucleobase-Rich Extract from Cordyceps Sinensis Inhibits the Epithelial–Mesenchymal Transition and Protects against Renal Fibrosis in Diabetic Nephropathy

“…Diabetic nephropathy is featured as a progressive renal failure in combination with the augmented deposition of ECM proteins, leading to mesangial expansion, glomerulosclerosis, and atrophy [31]. From a macroscopic viewpoint, abnormal changes of renal function are mainly manifested as significant increases in kidney indexes, Alb, SCR, BUN, and TC during the development and progression of DN [32,33,34]. Tubulointerstitial fibrosis (TIF), a critical change for the progression of diabetic nephropathy to kidney failure, has been shown to be a consistent predictor of functional impairment [35].…”