Effect of 2-Hydroxy-4-methoxy Benzoic Acid Isolated from Hemidesmus indicus on Erythrocyte Membrane Bound Enzymes and Antioxidant Status in Streptozotocin-induced Diabetic Rats

从印度菝葜中分离得到的2-羟基-4-甲氧基苯甲酸对链脲佐菌素诱导的糖尿病大鼠红细胞膜结合酶和抗氧化状态的影响

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Abstract

In the present study, the effect of 2-hydroxy-4-methoxy benzoic acid isolated from roots of Hemisdesmus indicus on the erythrocyte membrane bound enzymes and antioxidant status in streptozotocin-induced diabetic rats was investigated. The streptozotocin-induced diabetic rats were treated with 2-hydroxy-4-methoxy benzoic acid (500 μg/kg/day) for 7 weeks by oral intubation and compared with glibenclamide, a standard hypoglycemic agent (100 mg/kg). The erythrocyte membrane was isolated and the activity of Na(+)/K(+)-dependent ATPases, Ca(2+)-ATPases, Mg(2+)-ATPases were determined. Superoxide dismutase, catalase, glutathione peroxidase, glutathione-S-transferase, vitamins C, vitamin E, plasma reduced glutathione and erythrocyte glutathione, reduced glutathione content in the tissues was also assayed. Administration of 2-hydroxy-4-methoxy benzoic acid to diabetic rats significantly (F>0.05 and P<0.001) elevated the activity of total ATPases, Na(+)/k(+) ATPase, Mg(2+) ATPase and Ca(2+) ATPase to near normal level. The activities of catalase, superoxide dismutase and glutathione peroxidase and glutathione-S-transferase in erythrocytes were decreased significantly (F>0.05; P<0.001) in diabetic rats. Diabetic rats treated with 2-hydroxy-4-methoxy benzoic acid showed a significant (F>0.05; <0.001) increase in the enzymic antioxidants in erythrocytes. The elevated levels of vitamin E and low level of vitamin C and glutathione level in plasma and erythrocytes were observed in diabetic rats when compared to control rats and were restored significantly (F>0.05; P<0.001) after the administration of 2-hydroxy-4-methoxy benzoic acid. This study concludes administration of 2-hydroxy-4-methoxy benzoic acid supports the restoration of antioxidant defence, reduces the free radial production, lipid peroxidation and the glycosylation of haemoglobin in diabetic rats.

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