Antidiabetic and aldose reductase inhibitory potentials of Land caltrops aqueous extract in streptozotocin-nicotinamide induced diabetic rats

Document Type

Article

Publication Title

Journal of HerbMed Pharmacology

Abstract

Introduction: Diabetic retinopathy is a late stage complication in diabetic patients and one which dramatically affects quality of life. Persistent hyperglycemia results in sorbitol accumulation due to increased activity of aldose reductase (AR), which leads to changes in membrane permeability and leakage of glutathione (GSH) from the lens which in turn results in the development of cataract and retinopathy. Hence, the present study was designed to assess the effect of Tribulus terrestris on AR activity and GSH level in diabetic rat lens, random blood glucose, hemoglobin A1c (HbA1c) and insulin. Methods: Diabetes mellitus was induced by intra-peritoneal (i.p) injection of streptozotocin-nicotinamide (STZ-NA). Animals were divided into 5 groups including normal controls (NC) treated with saline, untreated diabetic controls (DC), T. terrestris (150 and 300 mg/kg) and glibenclamide (500 µg/kg) treated diabetic rats. After 16 weeks of treatment, the rats were sacrificed, the lens was removed through posterior approach and homogenate was prepared for AR activity estimation. The lens tissue homogenate was prepared in normal saline for the estimation of GSH. Blood glucose was estimated by glucometer, HbA1c by nephelometry and insulin by ELISA kit. Results: AR activity was significantly reduced (P<0.004) in T. terrestris (both doses) treated groups compared to untreated diabetic controls. GSH levels were found significantly higher (P<0.005) in treated groups than the ones in diabetic controls. Glucose, HbA1c and insulin were significantly improved (P<0.004) in plant extract treated groups when compared to untreated diabetic rats. Conclusion: Tribulus terrestris aqueous extract may be useful as AR inhibitor. It also has antioxidant and antidiabetic activities and thereby might be capable of controlling the hyperglycemia induced tissue damage.

First Page

218

Last Page

222

DOI

10.34172/jhp.2020.28

Publication Date

1-1-2020

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