Aydin Fatih, Kalaz Esra Betul, Kucukgergin Canan, Coban Jale, Dogru-Abbasoglu Semra, Uysal Mujdat
Department of Biochemistry, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey.
Department of Biochemistry, Yeditepe University Medical Faculty, Istanbul, Turkey.
Curr Aging Sci. 2018;11(1):10-15. doi: 10.2174/1871530317666170703123519.
Chronic administration of D-galactose (GAL) induces changes that resemble natural aging in rodents. Oxidative stress and Advanced Glycation End products (AGE) formation play a role in GAL-induced aging. Carnosine (CAR; β-alanyl-L-histidine) has antioxidant and anti-glycating actions and may be a potential therapeutic agent in aging due to these properties. The effect of CAR supplementation on AGE levels and oxidative stress parameters was investigated in serum, liver and brain tissues in GAL-treated rats.
GAL (300 mg/kg; s.c.; 5 days per week) alone or together with CAR (250 mg/kg/daily; i.p.; 5 days per week) was applied to male rats for two months. AGE, Advanced Oxidized Protein Products (AOPP), Protein Carbonyl (PC) and Malondialdehyde (MDA) levels together with Reactive Oxygen Species (ROS) formation and Ferric Reducing Antioxidant Power (FRAP) values were determined.
GAL treatment elevated AGE levels, ROS formation and protein and lipid oxidation products in serum and examined tissues. CAR treatment was observed to decrease significantly glycooxidative stress in serum, liver and brain tissues of GAL-treated rats.
Our results indicate that CAR may be useful for decreasing oxidative stress and glycation products in GAL-induced aging model in rats.
长期给予D-半乳糖（GAL）可诱导啮齿动物出现类似自然衰老的变化。氧化应激和晚期糖基化终产物（AGE）的形成在GAL诱导的衰老过程中起作用。肌肽（CAR；β-丙氨酰-L-组氨酸）具有抗氧化和抗糖化作用，基于这些特性，它可能是一种潜在的抗衰老治疗药物。本研究探讨了补充CAR对GAL处理大鼠血清、肝脏和脑组织中AGE水平及氧化应激参数的影响。
将雄性大鼠分为三组，分别给予单独的GAL（300 mg/kg；皮下注射；每周5天）、GAL与CAR联合处理（250 mg/kg/天；腹腔注射；每周5天），持续两个月。检测AGE、晚期氧化蛋白产物（AOPP）、蛋白质羰基（PC）、丙二醛（MDA）水平以及活性氧（ROS）生成量和铁还原抗氧化能力（FRAP）值。
GAL处理可提高血清及所检测组织中的AGE水平、ROS生成量以及蛋白质和脂质氧化产物。观察发现，CAR处理可显著降低GAL处理大鼠血清、肝脏和脑组织中的糖氧化应激。
我们的结果表明，CAR可能有助于降低GAL诱导的大鼠衰老模型中的氧化应激和糖化产物。
