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⁻¹ day⁻¹) 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.

中文翻译：

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肌肽通过改善SAMP8小鼠的线粒体功能障碍来改善与年龄有关的痴呆

痴呆是一种与年龄有关的神经退行性疾病。肌肽是由β-丙氨酸和L-组氨酸组成的内源性二肽，已显示具有神经保护作用。但是，确切的机制仍然不清楚。在这项研究中，使用了衰老加速小鼠易发8（SAMP8）小鼠，这是一种与年龄相关的动物模型。肌肽（100和200 mg千克^-1天^-1每天一次对小鼠口服给药，持续六周。行为测试，蛋白质印迹和检测试剂盒用于评估肌肽对SAMP8小鼠的潜在影响。旷野和新物体识别实验表明，肌肽改善了SAMP8小鼠的认知缺陷。肌肽可降低SAMP8小鼠的丙二醛（MDA）和活性氧（ROS）水平，超氧化物歧化酶（SOD）活性和三磷酸腺苷（ATP）水平。同时，Western印迹结果证明肌肽在SAMP8小鼠海马中增加了Mitofusin-1，Mitofusin-2和Bcl-2的蛋白表达，并降低了P-Drp1，Bax，Caspase-3和NLRP3炎性小体的蛋白表达。 。