Protective Effect of Acetylcysteine, Histidine, and Their Combination Against Diabetes Vascular Complications in Type-2 Diabetic Rats Via Reducing Nf-Kβ Pathway Signaling Publisher



Mahdavifard S¹ ; Nakhjavani M² Show Affiliations
Source: Journal of Diabetes and Metabolic Disorders Published:2022

Abstract

Purpose: The nuclear factor-kappa B (NF-κB) signaling participates in diabetes complications. Therefore, the reduction of NF-κB signaling may be a goal to prevent or improve them. Thus, we investigated the effects of acetylcysteine (AC), histidine (His), and their combination on the NF-κB expression and its different activators in type 2 diabetic rats. Methods: The survey was performed on 50 rats that were allotted equally into five groups composed of control, diabetic, diabetic treated with (AC, 0.06%), (His, 0.1%), and (AC & His) groups. Treated groups have received the treatments daily in drinking water for two months. Metabolic profile (glucose, insulin resistance indices, lipid profile, and cardiovascular indices) and renal dysfunction parameters (creatinine and urinary protein excretion) were measured. Plus, diverse glycation (early, intermediate, and end), oxidative stress (Oxidized LDL, Reduced glutathione), and inflammatory markers (interleukine-1β, myeloperoxidase, and NF-kβ expression) were determined. Results: Glucose, insulin resistance indices, cardiovascular indices, renal dysfunction parameters, different markers of glycation, oxidative stress, and inflammation as well as NF-κB expression, were the lowest in the (AC & His) treated diabetic rats. Besides, the cited parameter was lower in the Ac treated one than His treated (p > 0.001). Conclusion: The combination of AC and His had the most protective effect against diabetes complications and advantageous effect on metabolism, β-cell activity, and insulin function due to the most reductive effect on the NF-κB pathway rather than More than any of the amino acids alone. © 2022, The Author(s), under exclusive licence to Tehran University of Medical Sciences.