Elucidation of the role of calpain on the degeneration of spines caused by diabetes using a low molecular weight compound

慢性高血糖，如糖尿病，已被证明会导致认知障碍和海马区长时程增强缺陷。为了探讨高血糖引起认知损害的机制，本研究观察了人神经母细胞瘤细胞系SH-SY5Y在高糖暴露后突触后密度95(PSD-95)的表达以及链脲佐菌素诱导的糖尿病小鼠海马区突触后密度95(PSD-95)的表达。这些结果提示，在体内和体外慢性高血糖的不良反应中，磷酸化ERK的减少起着重要作用。

Chronic hyperglycemia, such as diabetes mellitus, has been shown to induce cognitive impairment and defects of long-term potentiation in the hippocampus. In order to assess the mechanism of cognitive impairment by hyperglycemia, the expression of post-synaptic density 95 (PSD-95), a key components of spine, was investigated in a human neruoblastoma cell line, SH-SY5Y, after exposure to high-glucose and in the hippocampus in streptozotocin-induced diabetic mice. These results suggest that decrease in phosphorylated ERK plays a significant role in the adverse effect of chronic hyperglycemia in vivo and in vitro.