Summary: | 碩士 === 中山醫學大學 === 生化暨生物科技研究所 === 96 === Diabetic ophthalmopathy is the leading cause of acquired blindness in the world. Diabetes sustained hyperglycemia circumstances, produced abnormal metabolism products to influence eye normal function, besides decreased antioxidant system, and furthermore produced free radical to damage eye.
It was demonstrated that Hibisus Sabdariffa potentiated antioxidative effect in previous studies. In this study, we further examined the effect of HSE or HPE on anti-ophthalmopathy. In Sprague-Dawley (SD) Rat experiment, after diabetes induction completed, HSE (100,200 and 300mg/kg), HPE (100,200 and 300 mg/kg) were fed by oral tube for nine weeks to observe the effects on diabetic rats. The results showed that treatment of HSE&HPE (100, 200 and 300 mg/kg) did not restrain the blood glucose. However, 100, 200 and 300mg/kg of HSE increased catalase activity to 13.2%, 10.1%, 13.8% ; and glutathione was increased to 9.2%, 8.2%, 8.4%. In the groups treated with 200 and 300mg/kg of HPE, catalase activity was increased to 4.4%, 3.3%; and glutathione was increased to 28%, 78%. In lens, HSE could decelerate the development of diabetic cataract by empiricism. In histopathological evalution of retina, HSE and HPE decreased diabetes induced retinal injury. We also found that in eye tissues, HSE or HPE cannot affect phosphorylation of Akt, but downregulate phosphorylation of extracellular signal-regulated kinase (ERK), p38 and JNK to reduce apoptosis. In retinal pigment epithelial (RPE) cell experiment, cell was pretreated with 200 μM of H2O2 accompanied with HSE or HPE (0.5, 1, 2, 3 mg/mL) for 6 hrs. The results showed that HPE could protect RPE cell from H2O2 induced damage . We also found HPE cannot affect phosphorylation of Akt, but downregulate phosphorylation of extracellular signal-regulated kinase (ERK) to reduce apoptosis.
In conclusion, we have demonstrated that HPE or HSE could have potential benefits in inhibiting diabetes induced ophthalmopathy.
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