Background: Diabetes mellitus is a metabolic disorder, leading to many complications. Cataract is important complication causing impairment of vision. Many factors play a role in cataract formation in diabetic individuals. Only treatment for cataract is surgery, having limitations. There is a need to explore for inexpensive, non-surgical approaches for prevention of cataract. The present study was planned to evaluate the effect of Nishamalaki (NA) on diabetic cataract.
Aims and Objectives: This study aims to study the prophylactic and therapeutic effect of NA on cataract and its mechanism of action.
Materials and Methods: Diabetes was induced in 42 Wistar rats with low-dose streptozotocin (STZ) followed by high-fat high-fructose diet. NA treatment initiated in six rats immediately after STZ administration (NA prophylactic Group II). Once diabetes was developed rats divided into six groups and received respective treatment for 8 weeks: Group I diabetic control, Group III NA therapeutic, Group IV glimepiride, Group V chloramphenicol, Group VI glutamine, and Group VII epalrestat. Then, estimation of aldose reductase (AR) and antioxidant enzymes in blood and lens was done.
Results: In Group I, cataract was initiated in the 2nd week and progressed to Stage 3 or 4 by the 8th week. No cataract was developed in NA prophylactic and chloramphenicol group. Delayed initiation and progression were seen in NA therapeutic and epalrestat, compared to glimepiride and glutamine group. NA was seen to work by antihyperglycemic, antioxidant, AR inhibition, and probably by CYP 450 inhibition.
Conclusion: NA is useful in the prevention and treatment of cataract in diabetic animals, working through many mechanisms.
Key words: Diabetes Mellitus; Cataract Score; Oxidative Stress; Nishamalaki
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