脂质、蛋白衍生毒性分子和抗氧化剂缺乏在2型糖尿病视网膜病变(DR)发病机制中的作用

Subhasish Pramanik, L. Mondal, S. Chowdhury, Chiranjit Bose, Debgopal Bera, Koena Bhattacharjee
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引用次数: 1

摘要

探讨nadph氧化酶介导的不同脂质、蛋白衍生分子的形成以及玻璃体中维生素c水平的降低在2型糖尿病(T2DM)中内皮功能障碍诱导的血管内皮生长因子分泌和糖尿病视网膜病变(DR)发病机制中的作用。对14例T2DM合并轻度非增殖性糖尿病视网膜病变(MNPDR)、11例非糖尿病视网膜病变(DNR)、17例T2DM合并高危增殖性糖尿病视网膜病变(HRPDR)和5例健康无糖尿病患者进行玻璃体分析,测定NADPH氧化酶、脂质过氧化如丙二醛(MDA)、4-羟基壬醛(HNE)和晚期脂质氧化终产物(ALE)如己醇赖氨酸(HLY)、蛋白羰基化合物(PCC)、采用标准分光光度法和酶联免疫吸附法(ELISA)测定维生素c和血管内皮生长因子(VEGF)分泌浓度。不同等级的DNR和DR患者玻璃体中nadph氧化酶、不同蛋白质和脂质源性分子、VEGF的浓度较HC组明显升高,而不同等级DR和DNR组玻璃体中维生素c水平较健康组明显降低。氧化应激介导的脂质和蛋白源性生物分子不仅在DR的发病机制中增加了重要的介质,而且加速了微血管病变的进展和严重程度。
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Role of Lipid, Protein-Derived Toxic Molecules, and Deficiency of Antioxidants behind the Pathogenesis of Diabetic Retinopathy (DR) in Type 2 Diabetes Mellitus
To determine the role of NADPH-oxidase mediated formation of different lipid, protein-derived molecules, and depletion of vitamin-C level in vitreous behind the endothelial dysfunction-induced vascular endothelial growth factor secretion and pathogenesis of diabetic retinopathy (DR) in type 2 diabetes mellitus (T2DM). Fourteen T2DM patients with mild non-proliferative diabetic retinopathy (MNPDR), 11 patients without diabetic retinopathy (DNR), 17 T2 DM subjects with high-risk proliferative diabetic retinopathy (HRPDR), and 5 healthy individuals without DM underwent vitreous analysis for estimation NADPH oxidase, lipid peroxide like malondialdehyde (MDA), 4-Hydroxy-noneal (HNE) and advanced lipoxidation end product (ALE) like Hexanoyl-lysine (HLY), protein carbonyl compound (PCC), Vitamin-C and concentration of vascular endothelial growth factor (VEGF) secretion following standard spectrophotometric methods and enzyme-linked immunosorbent assay (ELISA). Vitreous concentration of NADPH-oxidase, different protein and lipid-derived molecule, and VEGF were found to be significantly elevated among DNR and of DR subjects with different grades compared to HC subjects whereasthe vitamin-C level was found to be decreased among different DR subjects and DNR subjects in comparison to healthy individuals. Oxidative stress-mediated lipid and protein-derived biomolecules not only add important mediators in the pathogenesis of DR, but also accelerate the progression and severity of microangiopathy.
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