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Lycopene attenuates endothelial dysfunction in streptozotocin-induced diabetic rats by reducing oxidative stress.

机译:番茄红素通过减少氧化应激减轻链脲佐菌素诱导的糖尿病大鼠的内皮功能障碍。

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CONTEXT: Diabetes mellitus is characterized by oxidative stress, which in turn induces endothelial dysfunction. As a potent antioxidant compound, lycopene might rescue diabetic endothelial dysfunction by reducing oxidative stress. OBJECTIVE: The present study investigated whether lycopene could lower oxidative stress and attenuate endothelial dysfunction in diabetic rats. METHODS: Different doses of lycopene (10, 30, and 60 mg/kg/day, p.o.) were administered for 30 days to streptozotocin (STZ) (60 mg/kg)-induced diabetic rats. Biochemical parameters and aortic malondialdehyde (MDA) content, superoxidase dismutase (SOD) activity, nitric oxide (NO) levels, constitutive NOS (cNOS) activity, and inducible NOS (iNOS) activity were determined. Endothelium-dependent and endothelium-independent vasorelaxation were measured in aortas for estimating endothelial function. RESULTS: Compared with normal controls, endothelial function was significantly reduced in diabetic rats and the blunted endothelial function was dependently ameliorated with lycopene treatment. Compared with normal controls, the serum oxidized low-density lipoprotein (ox-LDL) levels, the aortic MDA levels, and iNOS activity in diabetic rats were increased by 113, 197, and 100%, respectively, whereas aortic SOD activity, NO levels, and cNOS activity were decreased by 73, 53, and 65%, respectively. Exogenous administration of lycopene to diabetic rats caused a dose-dependent decrease of serum glucose and ox-LDL levels, an increase of aortic SOD activity, NO levels, and cNOS activity, and a decrease of aortic MDA levels and iNOS activity. CONCLUSION: Chronic lycopene treatment could attenuate endothelial dysfunction by reducing oxidative stress in STZ-induced diabetic rats. These results indicate that chronic lycopene treatment might be useful in preventing diabetic vascular complications associated with endothelial dysfunction.
机译:背景:糖尿病的特征是氧化应激,进而引起内皮功能障碍。番茄红素作为有效的抗氧化剂化合物,可以通过降低氧化应激来缓解糖尿病性内皮功能障碍。目的:研究番茄红素是否可以降低糖尿病大鼠的氧化应激并减轻其内皮功能障碍。方法:对链脲佐菌素(STZ)(60 mg / kg)诱导的糖尿病大鼠给予30天不同剂量的番茄红素(10、30和60 mg / kg /天,口服)。测定生化参数和主动脉丙二醛(MDA)含量,超氧化物酶歧化酶(SOD)活性,一氧化氮(NO)水平,组成型NOS(cNOS)活性和诱导型NOS(iNOS)活性。在主动脉中测量内皮依赖性和非内皮依赖性血管舒张以估计内皮功能。结果:与正常对照组相比,糖尿病大鼠的内皮功能显着降低,番茄红素治疗可显着改善钝化的内皮功能。与正常对照组相比,糖尿病大鼠的血清氧化低密度脂蛋白(ox-LDL)水平,主动脉MDA水平和iNOS活性分别增加了113%,197%和100%,而主动脉SOD活性,NO水平和cNOS活性分别降低了73、53和65%。对糖尿病大鼠外源性番茄红素的给药导致剂量依赖性的血清葡萄糖和ox-LDL水平降低,主动脉SOD活性,NO水平和cNOS活性增加,以及主动脉MDA和iNOS活性降低。结论:慢性番茄红素治疗可通过减轻STZ诱导的糖尿病大鼠的氧化应激减轻内皮功能障碍。这些结果表明,慢性番茄红素治疗可能对预防与内皮功能障碍有关的糖尿病血管并发症有用。

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