Rhodopsin is the G protein-coupled receptor in rod photoreceptor cells that initiates vision upon photon capture. The light receptor is normally locked in an inactive state in the dark by the covalently bound inverse agonist 11-cis retinal. Mutations can render the receptor active even in the absence of light. This constitutive activity can desensitize rod photoreceptor cells and lead to night blindness. A G90D mutation in rhodopsin causes the receptor to be constitutively active and leads to congenital stationary night blindness, which is generally thought to be devoid of retinal degeneration. The constitutively active species responsible for the night blindness phenotype is unclear. Moreover, the classification as a stationary disease devoid of retinal degeneration is also misleading. A transgenic mouse model for congenital stationary night blindness that expresses the G90D rhodopsin mutant was examined to better understand the origin of constitutive activity and the potential for retinal degeneration. Heterozygous mice for the G90D mutation did not exhibit retinal degeneration whereas homozygous mice exhibited progressive retinal degeneration. Only a modest reversal of retinal degeneration was observed when transducin signaling was eliminated genetically, indicating that some of the retinal degeneration occurred in a transducin-independent manner. Biochemical studies on purified rhodopsin from mice indicated that multiple species can potentially contribute to the constitutive activity causing night blindness.

In this study, a molecular docking was performed on EGFR tyrosine kinase with plant phenolic compounds kaempferol, chrysophanol and emodin; identified from Cassia tora, an edible plant employed for eye diseases traditionally. The results illustrated that all the compounds have strong binding abilities with epidermal growth factor receptor and validated the reported anticataractogenic potential of C. tora leaves. Further, the compounds also satisfied the criteria for being a drug through its structural features. Taken together, it was proposed that the compounds; kaempferol, chrysophanol and emodin might be helpful for further drug design and development and could be employed as efficient lead compounds in ophthalmic drug formulations.

The present study was undertaken to evaluate the efficacy of Cassia tora leaves, an edible plant traditionally used for eye ailments, in preventing experimental cataractogenesis. Cataract is the leading cause of irreversible visual impairment worldwide characterized by the cloudiness or opacification of the lens due to the disturbance of even distribution of lens proteins and lipids. A significant number of epidemiological studies have suggested the potential role of herbal medicine in the prevention of cataract by maintaining lens architecture. The study was conducted in neonatal rat pups of 8-10 days old with an ethyl acetate fraction of Cassia tora leaves (ECT) administered by gastric intubation. After 30 days, the animals were sacrificed and various parameters such as redox status and gene expressions were evaluated in lenses. ECT administration caused a significant decrease in the onset and maturation of cataract, potentiated antioxidant defense and normalized lens crystallin expression against cataract induced animals. HPLC and ESI-MS analysis of ECT revealed the presence of flavonoids and anthraquinones. Thus, the present study indicates the therapeutic potential of Cassia tora leaves in preventing cataract and the effect is endorsed by the presence of antioxidants in Cassia tora leaves.

Luteolin, a flavonoid present in leaves and stems of many plants finds mention in literature for beneficial effects on eyes. Presently, no reports are available on the in vivo anticataractogenic effect of luteolin. The current study was designed to evaluate the efficacy of luteolin on selenite-induced cataract models in vivo. The study consisted of three groups of Sprague Dawley rat pups 8-10 d old (Group I (Normal), Group II (Cataract induced), and Group III (Treatment)). Cataract was induced in Group II and Group III by a subcutaneous injection of sodium selenite (4 μg/g body weight) on the 10th day. Luteolin was administered orally from 8th day up to 12th day at a concentration of 1 μg/g body weight in Group III. After 30 d, lenses of treated animals showed normal morphology. Activities of antioxidant enzymes were increased and levels of reactive oxygen species were decreased in the luteolin-treated group when compared to the cataract-induced group. Increased Ca(2+) ATPase activity and lowered calcium level, caspase 3 activity and down-regulation of caspase 3 expression were seen in the treatment group when compared to the selenite group. Luteolin enhances the antioxidant potential and thereby lowers the oxidative damages to the lens. It also stabilizes the membrane integrity of the lens and maintains the ionic balance.