Diabetic retinopathy (DR) occurs in untreated diabetic patients due to the strong influence of oxidative stress. Bioflavonoids are well known for their antioxidant property. Morin, a bioflavonoid, has been demonstrated for its antioxidant as well as antidiabetic activity. Thus, this research work intended to determine the ameliorative impact of morin in DR rats using STZ-induced type 1 diabetic model. To induce type 1 diabetic in rats STZ (60 mg/kg) was administered intraperitoneally. Grouping of animals was done as described below (n = 6), where, group I – normal control, group II – diabetic control, group III – morin (25 mg/kg), group IV – morin (50 mg/kg), and group V – metformin (350 mg/kg) were used. All the animals underwent treatment for 60 days as given above. It was observed that supplementation of morin (25 and 50 mg/kg) showed a noteworthy decline in elevated serum glucose level. Moreover, decrease in the level of LPO and improved activity of endogenous antioxidants (GPx, CAT, and SOD) was observed in morin treated groups. It also notably drops the concentration of TNF-α, IL-1β, and VEGF in the tissue homogenate of the retina. Furthermore, it increased the retinal thickness and cell count in the ganglion cell layer of the retina in diabetic animals. Hence, we can conclude that morin encumbers the progression of DR in diabetic animals, which may be via antioxidant property and suppression of TNF-α, IL-1β, and VEGF.
The liver is the primary organ for metabolizing and eliminating foreign chemicals. When liver cells are exposed to large concentrations of dangerous substances, hepatocyte malfunction, membrane damage, and degradation may occur. Another chemical that can harm the liver is carbon tetrachloride (CCl4). CCl4 is converted into trichloromethyl radical [CCl3]- by several cytochrome P450 isoforms. [CCl3]- subsequently reacts with oxygen to generate trichloromethyl peroxyl radical [CCl3OO]- and induce lipid peroxidation in cell membranes. In this study, the mechanism by which a variety of recently identified medicinal plants display hepatoprotective activity against CCl4-induced liver injury is investigated. We find that animal models have been used in investigations of plant extracts. Herbal plants largely protect against CCl4-induced hepatotoxicity because their phytochemicals have an inhibitory nature. The antioxidant properties of phytochemicals can halt lipid oxidation and restrict the production of free radicals by inhibiting microsomal enzymes. They can also help liver cells in their fight against CCl4-induced inflammation by strengthening and fortifying them. The effectiveness of various herbs that are hepatoprotective and are thus plausible candidates for use in medicine must be confirmed. Experiments using entire plant extracts should be replaced with tests that pinpoint the active ingredients and assess the extracts’ effect on a variety of liver cell lines.
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