PurposeTo review current literature on the renin-angiotensin system (RAS)-mediated pathogenic mechanisms and therapeutic targets in ocular diseases.MethodsA comprehensive literature survey was performed on PubMed, Scopus, and Google Scholar databases published from 1977 to 2016. The search terms were a RAS, angiotensin, angiotensin receptor, prorenin, pro (renin) receptor, angiotensin converting enzyme inhibitor, angiotensin receptor blocker associated with ocular disorders like cataract, glaucoma, diabetic retinopathy (DR), macular degeneration, and uveitis. Articles were reviewed on the basis of the association between ocular disorders and RAS and relevant articles were discussed.ResultsThe literature revealed that the individual RAS components including renin, angiotensins, angiotensin converting enzymes, and RAS receptors have been expressed in the specific ocular tissues like retina, choroid, and ciliary body. The activation of both circulatory and local RAS potentiate the various inflammatory and angiogenic signaling molecules, including vascular endothelial growth factor (VEGF), extracellular signal-regulated kinase, and advanced glycation end products (AGE) in the ocular tissues and leads to several blinding disorders like DR, glaucoma, and macular degeneration. The classical and newer RAS inhibitors have illustrated protective effects on blinding disorders, including DR, glaucoma, macular degeneration, uveitis, and cataract.ConclusionsThe RAS components are present in the extrarenal tissues including ocular tissue and have an imperative role in the ocular pathophysiology. The clinical studies are needed to show the role of therapeutic modalities targeting RAS in the treatment of different ocular disorders.
In the present study, an ethanolic root-bark extract of Moringa oleifera (MO) was examined for its antiulcer potential in albino Wistar rats using two experimental models: ethanol-induced and pylorus ligation-induced gastric ulceration. The extract was orally administered at three different doses (150, 350, and 500 mg/kg) for 15 consecutive days. The antiulcer effects in rats treated with different doses of the extract and omeprazole (30 mg/kg, p.o.) were determined and compared statistically with the antiulcer effects in the control rats treated with saline (NaCl, 0.9%). The MO at doses of 350 and 500 mg/kg decreased the ulcer index significantly as compared to the control group (p < 0.01). The percentage protections against gastric ulcers were 82.58%, 85.13%, and 86.15% for MO doses of 150, 350, and 500 mg/kg, respectively, in the pylorus-ligated ulcer model and 55.75%, 59.33%, and 78.51%, respectively, in the ethanol-induced ulcer model. The MO significantly reduced the free acidity, total acidity, and ulcer index (p < 0.01) and increased the pH of gastric content compared with the control group. This study suggests that MO possesses valuable antiulcer, antisecretory, and cytoprotective activity. Thus, an ethanolic root-bark extract of Moringa oleifera can be used as source for an antiulcer drug.
Bauhinia variegata (Leguminosae) commonly known as Kachnar, is widely used in Ayurveda as tonic to the liver. The present work was carried out to assess the potential of Bauhinia variegata bark as hepatoprotective agent. The hepatoprotective activity was investigated in carbon tetrachloride (CCl 4 ) intoxicated Sprague-Dawley rats. Bauhinia variegata alcoholic Stem Bark Extract (SBE) at diŠerent doses (100 and 200 mg/kg) were administered orally to male Sprague-Dawley rats weighing between 100 120 g. The eŠect of SBE on the serum marker enzymes, viz., AST, ALT, ALP and GGT and liver protein and lipids were assessed. The extract exhibited signiˆcant hepatoprotective activity. Hence, B. variegata appears to be a promising hepatoprotective agent.
PurposeTo evaluate modes of cataractogenesis in the hypertensive state by using different hypertensive animal models, including fructose, cadmium chloride (CdCl2), Nω-nitro-l-arginine methyl ester (l-NAME), and two-kidney, one clip (2K1C) method.MethodsMale Sprague–Dawley albino rats (150–180 g) were divided into different groups, each group containing six animals. Hypertension was induced in animals via six weeks administration of fructose (10% solution in drinking water), CdCl2 (0.5 mg/kg/day, i.p.), and l-NAME (20 mg/kg/day, p.o.) in their respective groups and NaCl (0.9% solution in drinking water) in the 2K1C group. The Ramipril-treated group (2 mg/kg/day, orally) served as a standard group for the 2K1C animal model. Blood pressure was measured biweekly using non-invasive blood pressure system. The biochemical parameters in serum and eye lenses were evaluated after six weeks of the experimental protocol.ResultsHypertensive animal models showed significant induction of systolic and diastolic blood pressure and modulation of oxidative stress through depletion of antioxidants, including glutathione peroxidase, catalase, superoxide dismutase, glutathione, and elevation of malondialdehyde in serum and eye lenses. A significant elevation of ionic contents (Na+ and Ca2+) and reduction of total protein and Ca2+ ATPase activity in eye lenses were observed in all hypertensive animal models except l-NAME when compared with the normal group. The significant restoration of the antioxidants, Malondialdehyde (MDA) total protein, and ionic contents in the eye lenses concomitant with reduction of blood pressure were observed in the ramipril-treated group as compared to the 2K1C animal model. The results indicate that the fructose, CdCl2, and 2K1C models showed pronounced cataractogenic effects in the rat eye lenses.ConclusionBased on our findings, it can be concluded that systemic hypertension significantly increases the risk of cataract formation in the rat eyes via modulation of the antioxidant defense mechanism and electrolyte homeostasis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.