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Original Article



Protective effect of plumbagin ophthalmic suspension on diabetic cataract via restoration of lenticular oxidative stress and protein modification in STZ-Induced rats

Apurva Yadav,Rajesh Choudhary,Anshul Ram,Umashankar Nirmalkar,Jaya Shree,Swarnali Das Paul.



Abstract
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Backgrounds: Diabetic cataract is an ocular complication of diabetes mellitus characterized by lens opacification. Previous studies demonstrate the beneficial effects of plumbagin against ex vivo and in vivo models. In extension, the present study was designed to assess the protective action of plumbagin ophthalmic suspension against the in vivo streptozotocin (STZ)-induced diabetic cataract rat model.
Methods: The diabetic cataract was induced by a single intraperitoneal dose of STZ (60 mg/kg) to the Wistar albino rats (150-180 g, 15-18 weeks old). Animals were divided into four groups (n=6 animals in each group): Normal Control, Diabetic Cataract Control (placebo), and two treatment groups receiving topical plumbagin ophthalmic suspension at 0.01% w/v (Plg T1) and 0.05% w/v (Plg T2) twice daily (10:00 am and 5:00 pm) for 10 weeks. After completion of the protocol, cataract maturation was monitored via lens opacity scoring. Biochemical assessments of isolated lenses included oxidative stress markers and protein solubility profiles.
Results: Topical administration of plumbagin considerably prevents the progression of cataract maturation and maintains the lens transparency compared to the diabetic cataract control group. The results demonstrated that topical administration of plumbagin significantly (p < 0.05) elevated the lens antioxidant levels, such as catalase, superoxide dismutase, and glutathione, and reduced the lens malondialdehyde and nitrite content compared to the STZ control group. Moreover, plumbagin treatments significantly (p < 0.05) restored the lens protein content compared to the diabetic cataract control group.
Conclusion: Topical application of plumbagin effectively delays the progression of diabetic cataract in STZ-induced rats. The mechanism involves the mitigation of lenticular oxidative stress and the preservation of water-soluble crystallin proteins, suggesting plumbagin as a promising non-surgical therapeutic candidate for diabetic ocular complications.

Key words: Plumbagin; Anticataract activity; Diabetic cataract; Antioxidant activity







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