Abstract
The present research aimed at evaluating the protective role of betalain on the in vitro glaucoma model using PC12 neuronal cells. The cultured neuronal cells in a customized pressurized chamber were analyzed for the onset of glutathione, myeloperoxidase (MPO), cathepsin, expression of inflammatory enzymes such as cyclooxygenase (COX-1), lipoxygenase (5- LOX), sPLA2 caveolin-1, glaucoma markers and other inflammatory cytokines in the presence and absence of betalain. The results have shown that a significant increase in the expression of oxidative stress with increased activity of cathepsin B and D. On the other hand, the activity of inflammatory enzymes such as COX-1, 5- LOX, sPLA2 were significantly increased in pressure exposed cells. In addition, glaucoma simulated cells demonstrated a significant increase in the VEGF, TGF-β, BDGF, and neuroserpin compared to control. Moreover, cells predisposed to hydrostatic pressure demonstrated an increase in (p < 0.01) inflammatory cytokines such as IL-6, CXCR4, IL-17, IL-1β, and TNF-α levels. However, cells pre-treated with betalain improved the glutathione levels with attenuated MPO activity. Simultaneously, the levels of inflammatory cytokines and other glaucoma marker genes found restored in drug pre-treated cells. Thus, the results of the present study demonstrate that the use of betalain on ocular cells can prevent the progression of the disease that can be a suggestive therapeutic for controlling glaucoma like conditions.
Highlights
The optic neuropathy disease, glaucoma is defined by the loss of retinal ganglion cells and their axons that are complicated by the optic nerve head, and retinal tissue remodeling (Smith et al 2017) is progressive and multifactorial (Shahsuvaryan 2013) and is debilitating in the old age due to the blindness of the retina
The PC12 cells grown under hydrostatic pressures demonstrated the increased (p < 0.01) MPO with reduced levels of glutathione compared to control cells grown under no pressure
In our PC12 glaucoma model, the increase in oxidative stress may increase nitric oxide, which is an important mediator of the blood flow to the retina and helps ganglion cells to get nourishment
Summary
The optic neuropathy disease, glaucoma is defined by the loss of retinal ganglion cells and their axons that are complicated by the optic nerve head, and retinal tissue remodeling (Smith et al 2017) is progressive and multifactorial (Shahsuvaryan 2013) and is debilitating in the old age due to the blindness of the retina. Glaucomatous optic neuropathy takes time to develop, and the disease is known to be progressive. Patients suffering from this disease would be having difficulty in vision with a great decrease in the contrast and color sensitivity. Elevation of IOP compresses the retinal ganglion axons and affects the axonal transport for the delivery of nutrition to the survival of ganglions (Ster et al 2014) This may onset a mild reperfusion injury that would ensure inflammation and accelerate the production of free radicals and results in oxidative damage (Renner et al 2017). Ganglions may undergo apoptosis and results in the death of these cells and causes glaucomatous optic neuropathy in which oxidative stress has been implicated (Oharazawa et al 2010). Oxidative stress results in the imbalance in the antioxidant defenses to the levels of reactive oxygen species generated and has been suggested to cause retinal ischemic injury and in glaucoma pathogenesis (Kortuem et al 2000; Kuriyama et al 2001)
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