Oxymatrine impedes the progression of endotoxin-induced glaucoma via redox system modulations.

This study aimed to provide irrefutable evidence of the preventive effects of oxymatine (OMT) on a model of endotoxin induced glaucoma in Wistar rats which can be attributed to its anti-inflammatory, antioxidant, and TNF-α antagonistic properties. To assess the impact of OMT on uveitic glaucoma, the normal group received 100 µL distilled water topically for 15 days, while the glaucoma control group was induced with uveitic glaucoma by applying 10 µL of 10 µg/mL lipopolysaccharide (LPS) topically for 3 consecutive days. The treatment groups were then given OMT solution at a volume of 50 µL with varying doses of 0.25%, 0.5%, and 1% once a day via topical administration for 15 days. In addition, as a standard, the animals were also given 100 µL of 1% dorzolamide topically for 15 days. All ophthalmic dosing was carried out by pulling the lower eye-lid of the experimental animals and administration of the respective solutions. The study uses cutting-edge real-time imaging of the retinal vasculature in anesthetized animals, postsacrifice lenticular picturization and biochemical evidence to support the changes in the retinal layers. LPS induced animals demonstrated increased IOP, disrupted antioxidant systems, massive lipid damage, enhanced TNF-α activity and changes in intracellular ATPase and ionic activities. The damaged retinal vasculature and lenticular opacification further supported the biochemical evidence. However, using OMT at a 1% dosage effectively enhanced the antioxidant levels, regulated intracellular ion concentration and ATPases, decreased TNF-α activity, and counteracted mechanobiological changes in the visual front and retina. Moreover, OMT can successfully normalize intraocular pressure, making it a highly beneficial treatment option for glaucoma.

Oxymatrine Protects TGFß1-Induced Retinal Fibrosis in an Animal Model of Glaucoma.

Glaucoma has engulfed a huge population of the world into its claws of blindness as it remains asymptomatic until nearly 40% of the neurons are lost and the only option left is for patients to be subjected to symptomatic treatments or surgical methods, neither of which is completely effective in curing the disease as they do not restore the physiological dimensions at the neuronal level. Among the several factors that drive the pathophysiology of glaucoma, one is the involvement of fibrogenic factors, such as transforming growth factor ß (TGFß) which remodels the extracellular matrix (ECM) and, thus, the deposition of fibrotic material in the retina, resulting in the progression of primary open-angle glaucoma (POAG). The primary objectives of this study were to evaluate the protective effects of oxymatrine (OMT) in the steroid-induced glaucoma model in experimental rats and to determine the role of transforming growth factor ß1 (TGFß1) in the pathogenesis of glaucoma and its consequent inhibition due to the antioxidant and the antiinflammatory, and also the TGFß1 antagonistic, behavior of OMT. To that end, we experimentally elucidated the role of OMT, a TGFß1 antagonist, that is known to play antiinflammatory and antioxidant roles in the steroid-induced glaucoma model in experimental rats, and using the enzyme-linked immunosorbent assay (ELISA), we observed a direct inhibitory effect of OMT on the pathogenesis of glaucoma. The antioxidant and the antiinflammatory potentials of OMT were determined using several biochemical methods to determine the major antioxidants in the retinal layers, such as superoxide dismutase (SOD), glutathione peroxidase (GPX), catalase (CAT), and glutathione (GSH), along with the nitrite and the malondialdehyde (MDA) concentration levels. As a result, OMT was found to reduce the total protein content in the retinal layers, a correlation that has not been previously reported. Moreover, the impacts of OMT on the major governing ATPases, namely Na+/K+ ATPase and Ca2+ATPase, along with its impacts on the intracellular ionic concentrations of Na+, K+, and Ca2+, were determined and were found to point toward OMT, restoring homeostasis in glaucomatous animals. A clearer picture of the changes during the treatment was obtained using retinal images of the live animals and of the lenticular changes in the sacrificed animal; these images provided data on the pathological pathways leading to glaucoma inception and its consequent inhibition by OMT. The data reported in this study clearly indicate that OMT has a possible role in inhibiting the pathogenesis of glaucoma, and the data also permit the quantification of several biochemical parameters of concern.