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作 者:曹德寿[1] 谷春雨[2] 刘晓湘[3] 方秀斌[3]
机构地区:[1]中国医科大学解剖学教研室,辽宁省沈阳市110003 [2]中国医科大学附属第二临床学院神经外科,辽宁省沈阳市110001 [3]中国医科大学神经生物学教研室,辽宁省沈阳市110003
出 处:《中国临床康复》2004年第31期6914-6915,i002,共3页Chinese Journal of Clinical Rehabilitation
基 金:国家自然科学基金资助项目(30070330);辽宁省教育厅基金资助项目(20121032)~~
摘 要:目的:探讨细胞外信号调节激酶(extracellularsignal-regulatedkinase,ERK)信号转导途径在哮喘豚鼠初级传入神经元(C7~T5脊神经节)的作用及地塞米松的抑制作用。方法:健康白色豚鼠40只,随机分为4组:生理盐水组8只,单纯致敏组8只,哮喘组12只,地塞米松组12只,利用免疫组织化学结合显微图像分析,研究哮喘豚鼠C7~T5脊神经节活化的ERK免疫反应变化。结果:与生理盐水组(175.37±8.12)和单纯致敏组(173.57±5.67)相比,哮喘组豚鼠(148.53±8.56)活化ERK免疫反应在C7~T5脊神经节神经元的核中明显上调(t=20.532,t=20.201,P<0.01),其阳性细胞比率(84.50±4.02)%明显高于生理盐水组(19.43±3.88)%和单纯致敏组(21.20±2.05)%,地塞米松组豚鼠活化ERK免疫反应(168.18±8.17)在C7~T5脊神经节神经元的核中明显低于哮喘组(t=11.605,P<0.01)。结论:C7~T5脊神经节神经元中ERK的活化提示可能参与哮喘的发病过程,地塞米松抑制哮喘豚鼠C7~T5脊神经节神经元中ERK活化的表达为预防治疗哮喘及早期康复提供了新的可能途径。AIM:To explore the effect of extracellular signal-regulated kinase(ERK) signal transduction pathway and the inhibitory effect of dexamethasone on primary afferent neurons(C7-T5 spinal ganglia) of asthmatic guinea pigs. METHODS:Forty healthy white guinea pigs were randomly divided into 4 groups:saline group(n=8),simple sensitization group(n=8),asthma group(n=12) and dexamethasone group(n=12).The alterations of ERK immunoreactivity was investigated by means of immunohistochemistry combined with the micro-image analysis in C7-T5 spinal ganglia of asthmatic guinea pigs. RESULTS:The ERK immunoreactivity was increased significantly in nuclei of the C7-T5 spinal ganglion neurons in the asthma group(148.53±8.56) as compared with the saline group(175.37±8.12)and simple sensitization groups(173.57±5.67)(t=20.532,t=20.201,P< 0.01).The positive cell rate in the asthma group[(84.50±4.02)%] was obviously higher than those in the saline group[(19.43±3.88)%] and simple sensitization groups [(21.20±2.05)%].The ERK immunoreactivityin nuclei of the C7-T5 spinal ganglion neurons in the dexamethsone group(168.18±8.17)was much lower than that in the asthma group(t=11.605,P< 0.01). CONCLUSION:The activation of ERK in the C7-T5 spinal ganglion neurons may be involved in the pathogenesis of the bronchial asthma, and the inhibition of the expression of the ERK activation in these neurons may be a new way for prevention and early rehabilitation of bronchial asthma.
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