TROXERUTIN PREVENTS DIABETES AND DIABETIC ISCHEMIA INDUCED MEMORY DEFICITS AND BIOCHEMICAL CHANGES
Memory impairment induced by streptozotocin in rats is a consequence of changes in CNS that are secondary to chronic hyperglycemia, impaired oxidative stress, cholinergic dysfunction and interestingly, antihyperglycemics, antioxidants, and cholinergic agonists are reported to produce beneficial effect in this. Further, diabetes patients are susceptible to str oke induced memory deficits. Troxerutin, a trihydroxyethylated derivative of the natural bioflav onoid rutin is reported to exhibit anti-diabetic, antioxidant effect and acetylcholinesterase (AChE) inhibitor activity. It also exhibits anti -inflammatory and antithrombotic activity. However, no report is available on influence of troxerutin on streptoz otocin-induced memory impairment. Therefore, we tested its influence against cognitive dysfunction in streptozotocin-induced diabetic rats using object recognition paradigm. Lipid peroxidation and glutathione levels as parameters of oxidative stress and choline esterase (ChE) activity as marker of cholinergic function were assessed. Thirty days after diabetes induction rats showed a severe deficit in learning and memory associated with increased lipid peroxidation, decreased reduced glutathione, and elevated ChE activity. Further, chronic treatment with troxerutin (25-100mg/kg, p.o.) improved cognitive performance, lowered hyperglycemia, oxidative stress, and ChE activity in diabetic rats. Moreover, troxerutin also decreased brain infract size in diabetic ra ts. In conclusion, the present study is the first study to demonstrate that treatment with troxerutin prevents the changes in blood sugar levels, oxidative stress and ChE activity, and consequently memory impairment in diabetic rats.