Department of Neurology, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, China.
Food Funct. 2020 Mar 1;11(3):2489-2497. doi: 10.1039/c9fo02453k. Epub 2020 Mar 5.
Dementia is a kind of age-related neurodegenerative disease. Carnosine, an endogenous dipeptide consisting of β-alanine and l-histidine, has been shown to have neuroprotective effects. However, the exact mechanism is still obscure. In this study, senescence-accelerated mouse prone 8 (SAMP8) mice, an age-related animal model, were used. Carnosine (100 and 200 mg kg day) was orally administered to the mice once daily for six weeks. Behavioral tests, western blotting, and detection kits were used to evaluate the potential effects of carnosine on SAMP8 mice. Open-field and new object recognition experiments have shown that carnosine improved cognitive deficits in SAMP8 mice. Carnosine decreased the levels of malondialdehyde (MDA) and reactive oxygen species (ROS), increased the activity of superoxide dismutase (SOD) and the level of adenosine triphosphate (ATP) in SAMP8 mice. Concomitantly, western blotting results proved that carnosine increased the protein expressions of Mitofusin-1, Mitofusin-2, and Bcl-2 and reduced the protein expressions of P-Drp1, Bax, cleaved Caspase-3 and NLRP3 inflammasomes in the hippocampus of SAMP8 mice. The present data provided evidence that carnosine might improve cognitive impairment in SAMP8 mice through modulating mitochondrial dysfunction.
痴呆是一种与年龄相关的神经退行性疾病。肌肽，一种由β-丙氨酸和 l-组氨酸组成的内源性二肽，已被证明具有神经保护作用。然而，其确切的机制仍不清楚。在这项研究中，使用了快速老化模型小鼠 8 号（SAMP8），这是一种与年龄相关的动物模型。肌肽（100 和 200mg/kg/天）每天口服一次，共六周。行为测试、western blot 和检测试剂盒用于评估肌肽对 SAMP8 小鼠的潜在影响。旷场和新物体识别实验表明，肌肽改善了 SAMP8 小鼠的认知缺陷。肌肽降低了丙二醛（MDA）和活性氧（ROS）的水平，增加了 SAMP8 小鼠中超氧化物歧化酶（SOD）的活性和三磷酸腺苷（ATP）的水平。同时，western blot 结果证明肌肽增加了线粒体融合蛋白 1、线粒体融合蛋白 2和 Bcl-2 的蛋白表达，降低了 SAMP8 小鼠海马体中 P-Drp1、Bax、裂解 Caspase-3 和 NLRP3 炎性小体的蛋白表达。本数据提供了证据表明，肌肽可能通过调节线粒体功能障碍改善 SAMP8 小鼠的认知障碍。
