Ying Chang-jiang, Zhang Fang, Zhou Xiao-yan, Hu Xiao-tong, Chen Jing, Wen Xiang-ru, Sun Ying, Zheng Kui-yang, Tang Ren-xian, Song Yuan-jian
Department of Endocrinology, Affiliated Hospital of Xuzhou Medical College, Xuzhou, 221002, Jiangsu, People's Republic of China.
Laboratory of Morphology, Xuzhou Medical College, Xuzhou, 221004, Jiangsu, People's Republic of China.
Cell Mol Neurobiol. 2015 Oct;35(7):1027-37. doi: 10.1007/s10571-015-0197-3. Epub 2015 May 14.
Chronic inflammation appears to play a critical role in sickness behavior caused by diabetes mellitus. Astaxanthin has been used in treating diabetes mellitus and diabetic complications because of its neuroprotective and anti-inflammatory actions. However, whether astaxanthin can improve sickness behavior induced by diabetes and its potential mechanisms are still unknown. The aim of this study was to investigate the effects of astaxanthin on diabetes-elicited abnormal behavior in mice and its corresponding mechanisms. An experimental diabetic model was induced by streptozotocin (150 mg/kg) and astaxanthin (25 mg/kg/day) was provided orally for 10 weeks. Body weight and water consumption were measured, and the sickness behavior was evaluated by the open field test (OFT) and closed field test (CFT). The expression of glial fibrillary acidic protein (GFAP) was measured, and the frontal cortical cleaved caspase-3 positive cells, interleukin-6 (IL-6), and interleukin-1β (IL-1β) expression levels were also investigated. Furthermore, cystathionine β-synthase (CBS) in the frontal cortex was detected to determine whether the protective effect of astaxanthin on sickness behavior in diabetic mice is closely related to CBS. As expected, we observed that astaxanthin improved general symptoms and significantly increase horizontal distance and the number of crossings in the OFT and CFT. Furthermore, data showed that astaxanthin could decrease GFAP-positive cells in the brain and down-regulate the cleaved caspase-3, IL-6, and IL-1β, and up-regulate CBS in the frontal cortex. These results suggest that astaxanthin provides neuroprotection against diabetes-induced sickness behavior through inhibiting inflammation, and the protective effects may involve CBS expression in the brain.
慢性炎症似乎在糖尿病引发的疾病行为中起关键作用。虾青素因其神经保护和抗炎作用已被用于治疗糖尿病及糖尿病并发症。然而，虾青素是否能改善糖尿病诱发的疾病行为及其潜在机制仍不清楚。本研究的目的是探讨虾青素对小鼠糖尿病诱发的异常行为及其相应机制的影响。通过链脲佐菌素（150mg/kg）诱导建立实验性糖尿病模型，并口服给予虾青素（25mg/kg/天），持续10周。测量体重和饮水量，并通过旷场试验（OFT）和封闭场试验（CFT）评估疾病行为。检测胶质纤维酸性蛋白（GFAP）的表达，并研究额叶皮质裂解的半胱天冬酶-3阳性细胞、白细胞介素-6（IL-6）和白细胞介素-1β（IL-1β）的表达水平。此外，检测额叶皮质中的胱硫醚β-合酶（CBS），以确定虾青素对糖尿病小鼠疾病行为的保护作用是否与CBS密切相关。正如预期的那样，我们观察到虾青素改善了一般症状，并显著增加了旷场试验和封闭场试验中的水平距离和穿越次数。此外，数据显示虾青素可减少脑中GFAP阳性细胞，下调裂解的半胱天冬酶-3、IL-6和IL-1β，并上调额叶皮质中的CBS。这些结果表明，虾青素通过抑制炎症对糖尿病诱发的疾病行为提供神经保护，且保护作用可能涉及脑中CBS的表达。
