Chlorophytum alismifolium mitigates microvascular complications of type 2 diabetes mellitus: the involvement of oxidative stress and aldose reductase.

Chlorophytum alismifolium (C. alismifolium) tubers are used in the management of diabetes. This research evaluated the effect of ethylacetate extract of C. alismifolium (EACA) on microvascular complications and the possible association of oxidative stress and aldose reductase in type 2 diabetic rats. C. alismifolium tubers were subjected to sequential extraction until ethylacetate extract was obtained using a soxhlet apparatus. The LD₅₀ was determined using the OECD 425 guideline. The animals were placed on high fat diet for 42 days and then induced with hyperglycaemia using 40 mg/kg of streptozotocin. Diabetic neuropathy was evaluated using thermal and mechanical methods. Serum was used for the assessment of oxidative stress markers and biochemical markers of retinopathy and nephropathy. Serum aldose reductase was investigated by utilizing the principle of enzyme-linked immunosorbent assay. The median lethal dose of EACA was assessed to be above 5,000 mg/kg and it caused no mortality. Treatment with EACA significantly reduced the withdrawal times in both thermal and mechanical hyperalgesic methods (p<0.05). EACA also significantly reduced the levels of urea (p<0.001), albumin (p<0.05) and uric acid (p<0.001) in hyperglycaemic rats. EACA significantly decreased the amounts of low density lipoprotein and triglycerides (p<0.001). There was a remarkable elevation in the levels of high density lipoprotein (p<0.05). A significant (p<0.05) increase in the levels of magnesium was observed in the EACA-treated groups. EACA significantly increased catalase (p<0.05) and reduced malondialdehyde levels (p<0.05). The levels of aldose reductase was significantly (p<0.001) reduced by EACA compared to the hyperglycaemic control. The ethylacetate extract of C. alismifolium has beneficial effects in alleviating microvascular complications of diabetes through the inhibition of oxidative stress and aldose reductase in diabetic rats. [ABSTRACT FROM AUTHOR]