Acarbose, an α-Glucosidase Inhibitor, Maintains Altered Redox Homeostasis During Aging by Targeting Glucose Metabolism in Rat Erythrocytes

Abstract

Increasing age is the single largest risk factor for a variety of chronic illnesses. As a result, the capability to target the aging process has the potential to lead to increased health span. A lack of appropriate glucoregulatory control is a recurring issue associated with aging and chronic illness, even though many longevity therapies result in the preservation of glucoregulatory control. In this study, we suggest that targeting glucose metabolism to improve regulatory control can help to slow the aging process. Male Wistar rats, both young (age 4 months) and old (age 24 months), were given Acarbose (30mg/kg b.w.) for 6 weeks. An array of oxidative stress indicators was assessed after the treatment period, including plasma antioxidant capacity as determined by the ferric reducing ability of plasma (FRAP), reactive oxygen species (ROS), lipid peroxidation (MDA), reduced glutathione (GSH), total plasma thiol (SH), plasma membrane redox system (PMRS), protein carbonyl (PCO), advanced oxidation protein products (AOPPs), advanced glycation end products (AGEs), and sialic acid (SA) in control and treated groups. When compared to controls, acarbose administration increased FRAP, GSH, SH, and PMRS activities in both age groups. The treated groups, on the other hand, showed substantial decreases in ROS, MDA, PCO, AOPP, AGE, and SA levels. The effect of Acarbose on almost all parameters was more evident in old-aged rats. Acarbose significantly increased PMRS activity in young rats, here the effect was less prominent in old rats. Our data supports the restoration of antioxidant levels in older rats following short-term Acarbose treatment. The findings corroborate the potential role of Acarbose as a putative CRM.