Protective effect of β-hydroxybutyrate on glutamate induced cell death in HT22 cells

被引:0
作者
Wang, Ying [1 ,2 ]
Liu, Ning [3 ]
Zhu, Weiwei [1 ]
Zhang, Kaihui [3 ]
Si, Jianping [2 ,4 ]
Bi, Meirong [1 ]
Lv, Xin [3 ]
Wang, Jiwen [2 ,5 ]
机构
[1] Shandong Univ, Jinan Cent Hosp, Dept Pediat, Jinan 250013, Peoples R China
[2] Shandong Univ, Qilu Hosp, Childrens Med Ctr, Brain Sci Res Inst,Dept Neurol, Jinan 250012, Peoples R China
[3] Shandong Univ, Qilu Childrens Hosp, Pediat Res Inst, Jinan 250022, Peoples R China
[4] Peoples Hosp Guangrao, Dept Pediat, Dongying 257300, Peoples R China
[5] Shanghai Jiao Tong Univ, Shanghai Childrens Med Ctr, Sch Med, Dept Neurol, 1678 Dongfang Rd, Shanghai 200127, Peoples R China
来源
INTERNATIONAL JOURNAL OF CLINICAL AND EXPERIMENTAL MEDICINE | 2016年 / 9卷 / 12期
关键词
beta-Hydroxybutyrate; glutamate; HT22; cells; KETOGENIC DIET; OXIDATIVE STRESS; KETONE-BODIES; IN-VIVO; EPILEPSY; ACETONE; ACETOACETATE; INCREASES; APOPTOSIS; ACID;
D O I
暂无
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
A ketogenic diet is a high-fat, adequate-protein, low-carbohydrate diet used in the treatment of paediatric epilepsy. However, little is known about the mechanism underlying its antiepileptic effect. Ketone bodies contain about 70% beta-hydroxybutyrate (BHB), a metabolic intermediate. Here, we sought to explore the protective effect of BHB on glutamate-induced toxicity in hippocampal neuronal HT22 cells and the underlying mechanisms. HT22 cells were pretreated with BHB, then exposed to glutamate. We examined cell viability, morphological characteristics of apoptosis, intracellular reactive oxygen species (ROS) levels, lipid peroxidation, and activation of the mitogen-activated protein kinase (MAPK) signal pathway. BHB significantly reduced the glutamate-decreased cell viability and inhibited HT22 cell death. Furthermore, BHB decreased ROS generation and alleviated lipid peroxidation. Exposure to glutamate strongly promoted the phosphorylation of c-Jun N-terminal kinase (JNK) and p38, and BHB reduced the glutamate-phosphorylated JNK and p38. MAPK signal pathways are essential for the neuroprotective effect of BHB on glutamate-induced toxicity in HT22 cells.
引用
收藏
页码:23433 / 23439
页数:7
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