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.

由于氧化应激的强烈影响，未治疗的糖尿病患者会发生糖尿病性视网膜病（DR）。生物类黄酮以其抗氧化性能而闻名。桑色素，一种生物类黄酮，已被证明具有抗氧化剂和抗糖尿病活性。因此，这项研究工作旨在使用STZ诱导的1型糖尿病模型来确定茉莉酸对DR大鼠的改善作用。为了在大鼠中诱导1型糖尿病，腹膜内给予STZ（60mg / kg）。动物分组如下所述（n = 6），其中，第一组–正常对照组，第二组–糖尿病对照组，第三组–莫林（25 mg / kg），第四组–莫林（50 mg / kg），第V组使用二甲双胍（350 mg / kg）。如上所述，所有动物均接受了60天的治疗。观察到补充的动蛋白（25和50 mg / kg）显示出血清葡萄糖水平升高的显着下降。此外，在用rinin处理的组中观察到了LPO水平的降低和内源性抗氧化剂（GPx，CAT和SOD）活性的提高。它还显着降低了视网膜组织匀浆中TNF-α，IL-1β和VEGF的浓度。此外，它增加了糖尿病动物的视网膜神经节细胞层中的视网膜厚度和细胞计数。因此，我们可以得出结论，morin会阻碍糖尿病动物的DR进程，这可能是通过抗氧化特性以及对TNF-α，IL-1β和VEGF的抑制作用引起的。它还显着降低了视网膜组织匀浆中TNF-α，IL-1β和VEGF的浓度。此外，它增加了糖尿病动物的视网膜神经节细胞层中的视网膜厚度和细胞计数。因此，我们可以得出结论，morin会阻碍糖尿病动物的DR进程，这可能是通过抗氧化特性以及对TNF-α，IL-1β和VEGF的抑制作用引起的。它还显着降低了视网膜组织匀浆中TNF-α，IL-1β和VEGF的浓度。此外，它增加了糖尿病动物的视网膜神经节细胞层中的视网膜厚度和细胞计数。因此，我们可以得出结论，morin会阻碍糖尿病动物的DR进程，这可能是通过抗氧化特性以及对TNF-α，IL-1β和VEGF的抑制作用引起的。