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Gentiopicroside attenuates diabetic retinopathy by inhibiting inflammation, oxidative stress, and NF-κB activation in rat model

机译:杜尼胆罗醇素通过抑制大鼠模型中的炎症,氧化应激和NF-κB活化来衰减糖尿病视网膜病变

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Diabetic retinopathy, an inflammatory condition, is one of the devastating complication associated with diabetes that can lead to irreversible blindness. Gentiopicroside (GP), a secoiridoid glycoside, exhibits anti-inflammatory and antioxidant activity. The investigation was carried out to explore whether GP could attenuate diabetic retinopathy in diabetic rats. Diabetes was induced by injecting streptozotocin (STZ) (65?mg/kg) intraperitoneally in 8-weeks-old male rats (200–240?g). The treatment group received GP (20, 40, 80?mg/kg) orally for a duration of 10?weeks in diabetic rats (n?=?10), and the diabetic group animals received phosphate buffer solution (n?=?20). Effect of GP on cell viability study was performed by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay. Oxidative stress markers, inflammatory mediators, and angiogenic factors were quantified in the retinal tissues of diabetic animals. All data were analyzed by one-way analysis of variance (ANOVA) at P ??0.05. Cytoprotective effect of GP was observed in MTT assay. GP effectively downregulated inflammatory cytokine, nuclear factor κB (NF-κB), tumor necrosis factor-α (TNF-α), interleukin 1 beta (IL-1β), and intercellular adhesion molecules-1 (ICAM-1), and upregulated antioxidant markers glutathione (GSH), superoxide dismutase (SOD), and catalase (CAT) in the retina of diabetic rats. GP equilibrated the disturbed angiogenic factors in the diabetic retinal tissues. Results clearly indicated defensive role of GP in the treatment of diabetic retinopathy by inhibition of NF-κB and oxidative stress.
机译:糖尿病视网膜病变,炎症状况,是与糖尿病相关的毁灭性并发症之一,可以导致不可逆转的失明。龙胆醇(GP),锡红外糖苷,表现出抗炎和抗氧化活性。进行调查以探索GP是否可以在糖尿病大鼠中衰减糖尿病视网膜病变。通过在8周龄雄性大鼠(200-240μg)中腹膜内腹膜内注射链脲佐菌素(STZ)(65×mg / kg)来诱导糖尿病。治疗组在糖尿病大鼠(n?= 10)中,在口服10?周的持续时间为10?=β=α10),并且糖尿病群动物接受磷酸盐缓冲溶液(n?= 20 )。 GP对细胞活力研究的影响由3-(4,5-二甲基-2-噻唑基)-2,5-二苯基-2H-四唑溴铵(MTT)测定进行。在糖尿病动物的视网膜组织中量化了氧化应激标记物,炎症介质和血管生成因子。通过单向分析(ANOVA)在p≤0.05时通过单向分析进行分析所有数据。在MTT测定中观察到GP的细胞保护作用。 GP有效下调炎症细胞因子,核因子κB(NF-κB),肿瘤坏死因子-α(TNF-α),白细胞介素1β(IL-1β)和细胞间粘附分子-1(ICAM-1),以及上调的抗氧化剂标记糖尿病大鼠视网膜中的谷胱甘肽(GSH),超氧化物歧化酶(SOD)和过氧化氢酶(猫)。 GP平衡糖尿病视网膜组织中干扰的血管生成因子。结果清楚地表明了GP在通过NF-κB和氧化应激治疗糖尿病视网膜病变治疗糖尿病视网膜病变的防御性作用。

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