Qin Suping, Sun Dexu, Mu Jingjing, Ma Daifu, Tang Renxian, Zheng Yuanlin
Key Laboratory for Biotechnology on Medicinal Plants of Jiangsu Province, School of Life Sciences, Jiangsu Normal University, Xuzhou, China.
Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou, Jiangsu, China.
Behav Brain Res. 2019 Feb 1;359:370-377. doi: 10.1016/j.bbr.2018.11.025. Epub 2018 Nov 19.
Hippocampal insulin resistance is the key factor in cognitive deficits. The obesity induces chronic inflammation and the inflammation molecules suppressors of cytokine signaling3 (SOCS3) and galectin-3 directly impair the insulin signaling. The anti-inflammation properties of purple sweet potato color (PSPC) prompted us to investigate the effect of PSPC on cognitive impairment associated with obesity. 60 C57BL/6 mice were randomly divided into four groups: normal, high fat diets (HFD), HFD+PSPC and PSPC. The mice were fed with the HFD or normal diet for 32 weeks. The PSPC (500 mg/kg/day) was administered via oral gavage from 21 to 32 weeks. The results showed the PSPC rectified the abnormal metabolism indexes induced by HFD, including ameliorated obesity, decreased the concentration of fasting blood glucose and improved the glucose tolerance. The Morris water maze test showed the PSPC alleviated the cognitive impairment in HFD mice. The PSPC decreased the expression of Iba1, tumor necrosis factor-α, interleukin-1β, SOCS3 and galectin-3 in hippocampus of HFD mice. The insulin signaling molecules including the p-IRS1 (Tyr608), PI3K p110α and p-AKT (Ser473) were detected and the PSPC treatment improved the insulin resistance in hippocampus of HFD mice. Furthermore, the PSPC increased Bcl-2, diminished the Bak and the cleaved-caspase3 in HFD mice hippocampus. These findings indicated that PSPC could be a potential treatment to improve the cognitive impairment associated with obesity.
海马体胰岛素抵抗是认知缺陷的关键因素。肥胖会引发慢性炎症，而炎症分子细胞因子信号传导抑制因子3（SOCS3）和半乳糖凝集素-3会直接损害胰岛素信号传导。紫甘薯色素（PSPC）的抗炎特性促使我们研究PSPC对与肥胖相关的认知障碍的影响。将60只C57BL/6小鼠随机分为四组：正常组、高脂饮食（HFD）组、HFD + PSPC组和PSPC组。给小鼠喂食HFD或正常饮食32周。从第21周到第32周，通过口服灌胃给予PSPC（500毫克/千克/天）。结果显示，PSPC纠正了由HFD诱导的异常代谢指标，包括改善肥胖、降低空腹血糖浓度和提高葡萄糖耐量。莫里斯水迷宫试验表明，PSPC减轻了HFD小鼠的认知障碍。PSPC降低了HFD小鼠海马体中Iba1、肿瘤坏死因子-α、白细胞介素-1β、SOCS3和半乳糖凝集素-3的表达。检测了包括p-IRS1（Tyr608）、PI3K p110α和p-AKT（Ser473）在内的胰岛素信号分子，PSPC治疗改善了HFD小鼠海马体中的胰岛素抵抗。此外，PSPC增加了HFD小鼠海马体中的Bcl-2，减少了Bak和裂解的caspase3。这些发现表明，PSPC可能是改善与肥胖相关的认知障碍的一种潜在治疗方法。
