Propofol inhibits growth of neurons through regulating insulin receptor and insulin-like growth factor-1 receptor

被引:0
作者
Gao, Sujie [1 ,2 ]
Chen, Xuebo [3 ]
Liu, Yingyi [2 ]
Wang, Jian [2 ]
Xu, Kaicheng [2 ]
Zhao, Guoqing [2 ]
Zhang, Guizhen [1 ]
机构
[1] Jilin Univ, Hosp 2, Ctr Lab, 218 Ziqiang St, Changchun 130041, Peoples R China
[2] Jilin Univ, China Japan Union Hosp, Dept Anesthesiol, Changchun, Peoples R China
[3] Jilin Univ, China Japan Union Hosp, Dept Gen Surg, 126 Xiantai Ave, Changchun 130021, Peoples R China
关键词
Propofol; neurotoxicity; insulin receptor; insulin-like growth factor-1 receptor; PI3K; AKT; RHESUS MACAQUE BRAIN; SEVOFLURANE ANESTHESIA; HIPPOCAMPAL-NEURONS; NEUROAPOPTOSIS; FETAL; RATS; PHOSPHORYLATION; NEUROPROTECTION; NEUROTOXICITY; RESISTANCE;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Neurotoxicity is a common side-effect of anesthetics. Propofol, as an anesthetic, is reported to induce apoptosis of neurons and lead to cognition and learning deficits. In our present study, we explored the effect of propofol on growth of neurons as well as the underlying mechanism in vivo and in vitro. We found that propofol inhibited the growth of neurons and influenced the protein level of the insulin receptor (IR) and Insulin-like growth factor-1 receptor (IGF-1R). Further mechanism study showed that, besides the reduction in receptor level of IR and IGF-1R, propofol activated PI3K-AKT signal and decreased the sensitivity of receptor, thus reducing glucose transporters (GLUTs) and inhibiting the growth of neuronal cells. Our study demonstrated that propofol inhibited the growth of neurons through the regulation of IR and IGF-1R. This study lays foundation for the exploration of propofol function as well as the employment of propofol in clinic.
引用
收藏
页码:6785 / 6794
页数:10
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