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Chlorogenic acid alters the voltage-gated potassium channel currents of trigeminal ganglion neurons

Chlorogenic acid alters the voltage-gated potassium channel currents of trigeminal ganglion neurons

作     者:Yu-Jiao Zhang Xiao-Wen Lu Ning Song Liang Kou Min-Ke Wu Fei Liu Hang Wang Jie-Fei Shen 

作者机构:State Key Laboratory of Oral Diseases West China Hospital of Stomatology Sichuan University Ningbo Dental Hospital 

出 版 物:《International Journal of Oral Science》 (国际口腔科学杂志(英文版))

年 卷 期:2014年第6卷第4期

页      面:233-240页

核心收录:

学科分类:1002[医学-临床医学] 100204[医学-神经病学] 10[医学] 

基  金:supported by the National Science Foundation of China (Grant No. 81000456) the Science and Technology Department of Sichuan Province (Grant No. 2009SZ0171) 

主  题:chlorogenic acid trigeminal ganglion neuron voltage gated potassium channel whole cell patch clamp 

摘      要:Chlorogenic acid(5-caffeoylquinic acid, CGA) is a phenolic compound that is found ubiquitously in plants, fruits and vegetables and is formed via the esterification of caffeic acid and quinic acid. In addition to its notable biological functions against cardiovascular diseases, type-2 diabetes and inflammatory conditions, CGA was recently hypothesized to be an alternative for the treatment of neurological diseases such as Alzheimer's disease and neuropathic pain disorders. However, its mechanism of action is ***-gated potassium channel(Kv) is a crucial factor in the electro-physiological processes of sensory neurons. Kv has also been identified as a potential therapeutic target for inflammation and neuropathic pain disorders. In this study, we analysed the effects of CGA on the two main subtypes of Kv in trigeminal ganglion neurons, namely, the IK,Aand IK,Vchannels. Trigeminal ganglion(TRG)neurons were acutely disassociated from the rat TRG, and two different doses of CGA(0.2 and 1 mmol·L21) were applied to the ***-cell patch-clamp recordings were performed to observe alterations in the activation and inactivation properties of the IK,Aand IK,Vchannels. The results demonstrated that 0.2 mmol·L21CGA decreased the peak current density of IK,A. Both 0.2 mmol·L21and1 mmol·L21CGA also caused a significant reduction in the activation and inactivation thresholds of IK,Aand IK,V. CGA exhibited a strong effect on the activation and inactivation velocities of IK,Aand IK,V. These findings provide novel evidence explaining the biological effects of CGA, especially regarding its neurological effects.

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