CD95在阿托伐他汀抗大鼠三叉神经痛中的作用机制  

Mechanism of CD95 in atorvastatin against trigeminal neuralgia of rats

作　　者：彭双春 陈米炼 欧册华 PENG Shuangchun;CHEN Milian;OU Cehua(Department of Pain,the Affiliated Hospital of Southwest Medical University,Luzhou 646000,Sichuan Province,China)

机构地区：[1]西南医科大学附属医院疼痛科,四川泸州646000

出　　处：《新乡医学院学报》2020年第1期26-29,共4页Journal of Xinxiang Medical University

基　　金：四川省卫生计生委科研课题(编号:6PJ567);泸州-川医大联合基金项目[编号:2015LZCYD-S06(4/11)]。

摘　　要：目的探讨CD95在阿托伐他汀抗大鼠三叉神经痛中的作用机制。方法雄性Sprague Dawley大鼠30只随机分为假手术组、三叉神经痛组和阿托伐他汀组,每组10只。三叉神经痛组和阿托伐他汀组大鼠结扎右侧眶下神经远端制备三叉神经痛模型,假手术组大鼠仅暴露右侧眶下神经,不结扎。造模后,阿托伐他汀组大鼠每天给予阿托伐他汀钙灌胃(10 mg·kg^-1),共14 d;假手术组、三叉神经痛组大鼠每天给予等体积生理盐水灌胃,共14 d。分别于造模前1 d及造模后3、7、14 d检测各组大鼠机械痛阈。造模后第15天处死大鼠取前额叶皮质,采用Western blot检测各组大鼠前额叶皮质中CD95、核因子-κB(NF-κB)、p-NF-κB、白细胞介素(IL)-1β蛋白表达量。结果造模前3组大鼠机械痛阈比较差异无统计学意义(P>0.05)。造模后3、7、14 d,三叉神经痛组和阿托伐他汀组大鼠机械痛阈低于假手术组(P<0.05);造模后3 d,三叉神经痛组和阿托伐他汀组大鼠机械痛阈比较差异无统计学意义(P>0.05);造模后7、14 d,阿托伐他汀组大鼠机械痛阈高于三叉神经痛组(P<0.05)。三叉神经痛组大鼠前额叶皮质中CD95、NF-κB、p-NF-κB、IL-1β蛋白表达量高于假手术组(P<0.05);阿托伐他汀组和假手术组大鼠前额叶皮质中CD95、NF-κB、p-NF-κB、IL-1β蛋白表达量比较差异无统计学意义(P>0.05);阿托伐他汀组大鼠前额叶皮质中CD95、NF-κB、p-NF-κB、IL-1β蛋白表达量低于三叉神经痛组(P<0.05)。结论阿托伐他汀可减轻三叉神经痛大鼠疼痛,其机制可能与抑制前额叶皮质中CD95、NF-κB、p-NF-κB、IL-1β蛋白表达,从而抑制前额叶皮质神经炎症有关。Objective To investigate the mechanism of CD95 in atorvastatin against trigeminal neuralgia of rats.Methods Thirty adult male Sprague Dawley rats were randomly divided into sham operation group,trigeminal neuralgia group and atorvastain group,with 10 rats in each group.The right infraorbital nerve of rats in trigeminal neuralgia group and atorvastain group was dissociated and ligated to prepare the trigeminal neuralgia model;the right infraorbital nerve of rats in sham operation group was dissociated without ligation.After modeling,the rats in atorvastain group were given atorvastatin calcium(10 mg·kg^-1)by intragastric administration daily for 14 days,the rats in sham operation group and trigeminal neuralgia group were given equivalent volume of normal saline daily for 14 days.The mechanical pain threshold of all rats was detected at 1 day before modeling and 3,7,14 days after modeling.At the 15 thday after modeling,all rats were sacrificed and the prefrontal cortex was reserved.The expressions of CD95,nuclear factor-κB(NF-κB),p-NF-κB and interleukin(IL)-1βprotein in the prefrontal cortex were detected by Western blot.Results There was no significant difference in mechanical pain threshold among the three groups before modeling(P>0.05).At 3,7,14 days after modeling,the mechanical pain threshold of rats in trigeminal neuralgia group and atorvastain group were lower than those in the sham operation group(P<0.05);at 3 days after modeling,there was no significant difference in mechanical pain threshold of rats between trigeminal neuralgia group and atorvastain group(P>0.05);at 7,14 days after modeling,the mechanical pain threshold of rats in the atorvastain group was higher than that in the trigeminal neuralgia group(P<0.05).The expressions of CD95,NF-κB,p-NF-κB and IL-1βprotein of rats in the trigeminal neuralgia group were higher than those in the sham operation group(P<0.05);there was no significant difference in the expressions of CD95,NF-κB,p-NF-κB and IL-1βprotein between the sham operation group an

关 键 词：CD95 阿托伐他汀 三叉神经痛 核因子-ΚB 

分 类 号：R651.3[医药卫生—外科学] R965[医药卫生—临床医学]