Affiliated TCM hospital/ Sino-Portugal TCM International Cooperation Center / Department of Physiology in School of Basic Medical Sciences, Southwest Medical University, Luzhou, 646000, China.
Hunan Provincial Research Center for Safety Evaluation of Drugs, Changsha, China.
Metab Brain Dis. 2019 Oct;34(5):1431-1446. doi: 10.1007/s11011-019-00448-7. Epub 2019 Jul 8.
The sedentary lifestyle is responsible for the high prevalence of diabetes which also impairs cognition including learning and memory. Various studies have highlighted the learning and memory impairments in rodent models but data regarding the timeline of their development and their correlation to biochemical parameters are scarce. So, the present study was designed to investigate the type of memory which is more susceptible to hyperglycemia and its correlation with biochemical parameters such as inflammatory cytokines, cAMP response element binding (CREB) and protein kinase B (Akt) activation. Hyperglycemia was induced using streptozotocin (STZ, 45 mg/kg i.p.) and confirmed by measuring fasting blood glucose levels after 1 week of STZ injection. Learning and memory deficits were evaluated using the Novel Object Recognition Test (NORT) and Morris water maze (MWM), and correlated with biochemical parameters (TNF-α, IL-1β, and dopamine) at 3, 6 and 9 weeks. STZ-injected rats after 3 weeks of injection demonstrated moderate hyperglycemia (blood glucose = 7.99 ± 0.62 mM) with intact learning and reference memory; however, their working memory was impaired in MWM. Severe hyperglycemia (blood glucose = 11.51 ± 0.69 mM) accompanied by impaired short, long, and working memory was evident after 6 weeks whereas learning was intact. After 9 weeks of STZ injection, hyperglycemia was more pronounced (13.69 ± 1.43 mM) and accompanied by a learning deficit in addition to short, long, and working memory impairments. The extent of hyperglycemia either in terms of duration or severity resulted in enhanced inflammation, down-regulation of the level of dopamine, protein expression of AKT and CREB, which possibly affected learning and memory negatively.
久坐的生活方式是导致糖尿病高发的原因,它还会损害认知能力,包括学习和记忆。各种研究都强调了啮齿动物模型中的学习和记忆障碍,但关于其发展的时间进程及其与生化参数的相关性的数据却很少。因此,本研究旨在研究哪种类型的记忆更容易受到高血糖的影响,并研究其与生化参数(如炎性细胞因子、cAMP 反应元件结合蛋白(CREB)和蛋白激酶 B(Akt)的激活)的相关性。通过腹腔注射链脲佐菌素(STZ,45mg/kg)诱导高血糖,并在 STZ 注射后 1 周测量空腹血糖水平来确认。使用新物体识别测试(NORT)和 Morris 水迷宫(MWM)评估学习和记忆缺陷,并与生化参数(TNF-α、IL-1β和多巴胺)在 3、6 和 9 周时进行相关性分析。在注射 STZ 3 周后,大鼠表现出中度高血糖(血糖=7.99±0.62mM),学习和参考记忆完整;然而,它们在 MWM 中的工作记忆受损。在注射 STZ 6 周后,出现严重高血糖(血糖=11.51±0.69mM),并伴有短期、长期和工作记忆受损,而学习是完整的。在注射 STZ 9 周后,高血糖更为明显(13.69±1.43mM),除了短期、长期和工作记忆受损外,还伴有学习障碍。高血糖的持续时间或严重程度都会导致炎症加剧,多巴胺水平下调,AKT 和 CREB 的蛋白表达减少,这可能会对学习和记忆产生负面影响。