Naringin protects against Bisphenol-A induced oculopathy as implication of cataract in hypertensive rat model.

People who have experienced high blood pressure are at greater risk of susceptibility to other health problems including oculopathy. The patients with these experiences do not have adequate treatment and those who do; spend much funds on the drug purchase. The study examines the protective effect of naringin (NRG) against ocular impairment in L-NAME induced hypertensive rat on exposure to a cellular disruptor. Fifty-six adult male albino rats were randomly distributed into eight (n = 7) groups. Group I: control animals, Group II was treated with Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME), Group III was treated with 50 mg/kg Bisphenol-A, Group IV was treated with L-NAME +50 mg/kg Bisphenol-A. Group V was administered with L-NAME +80 mg/kg NRG. Group VI was administered with 50 Mg/kg BPA + 80 mg/kg NRG. Group VII was administered with L-NAME+50 mg/kg Bisphenol-A +80 mg/kg NRG. Lastly, group VIII was treated with 80 mg/kg NRG alone for 14 days. Naringin prevented hypertension and ocular dysfunction by depleting the activities of angiotensin-converting enzymes, arginase, aldose-reductase and phosphodiesterase-51 (PDE-51) with corresponding down-regulation of inflammatory markers including TNF-α and IL-B. Moreover, ocular impairment was remarkably reduced by NRG as manifested by the decreased activities of AChE, BuChE, MAO-A and enzymes of ATP hydrolysis (ATPase, ADPase, AMPase) and adenosine deaminase with resultant increased NO level. Also, ocular expression of CD43 transcript, caspaace-9 and tumor suppressor P53 proteins were suppressed on treatment with NRG. This study corroborates the view that NRG may be a useful therapy in alleviating inflammatory markers, apoptosis and metabolic nucleotides disorders via the NOS/cGMP/PKG signaling pathways in hypertensive rat model on exposure to a cellular disruptor.