Department of Geriatrics, The First Affiliated Hospital, Chongqing Medical University, No.1 Youyi Road, Yuzhong District, Chongqing, 400016, China.
Inflammation. 2013 Dec;36(6):1286-94. doi: 10.1007/s10753-013-9667-2.
Ghrelin has a protective effect on diabetic encephalopathy. To expound the protective mechanism, we investigated the effects of ghrelin on high glucose-induced cell apoptosis and intracellular signaling in cultured PC12, which is a suitable model for studying neuronal cell death. High glucose-induced PC12 apoptosis was significantly inhibited by co-treatment of ghrelin. Sustaining inflammatory response is one of the molecular mechanisms of diabetic encephalopathy and TLR4 signaling has close relationship with inflammatory response. But there is no report about the biologic role of toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB) signaling in controlling high glucose-induced PC12 apoptosis by ghrelin. In this study, we found that TLR4/NF-κB pathway was activated by high glucose stimulation in PC12 and significantly alleviated by the co-treatment of ghrelin. From these findings, we made the conclusion that ghrelin could attenuate the symptoms of diabetic encephalopathy, which alleviates inflammatory reaction of diabetic encephalopathy by regulating TLR4/NF-κB pathway.
胃饥饿素对糖尿病性脑病具有保护作用。为了阐述其保护机制，我们研究了胃饥饿素对高糖诱导的培养 PC12 细胞凋亡及细胞内信号的影响，PC12 细胞是研究神经元细胞死亡的合适模型。高糖诱导的 PC12 细胞凋亡可被胃饥饿素的共同处理显著抑制。持续的炎症反应是糖尿病性脑病的分子机制之一，而 TLR4 信号与炎症反应密切相关。但目前尚无关于 TLR4/核因子-κB（TLR4/NF-κB）信号在胃饥饿素控制高糖诱导的 PC12 细胞凋亡中的生物学作用的报道。在这项研究中，我们发现 TLR4/NF-κB 通路在 PC12 中被高糖刺激激活，并被胃饥饿素的共同处理显著缓解。根据这些发现，我们得出结论，胃饥饿素可以减轻糖尿病性脑病的症状，通过调节 TLR4/NF-κB 通路减轻糖尿病性脑病的炎症反应。
