CAJ | 학술논문

目的观察偏头痛大鼠硬脑膜肥大细胞脱颗粒与神经源性炎症相关因子的变化,探讨偏头痛疼痛产生的可能机制.方法 64只SD大鼠随机分为刺激组(32只)和假手术组(32只).电刺激大鼠单侧三叉神经节建立偏头痛模型,放射免疫法测定刺激侧颈静脉血中降钙素基因相关肽(CGRP)的含量.酶联免疫吸附法测定刺激侧颈静脉血中组胺和硬脑膜中前列腺素E2(PGE2)的含量,甲苯胺蓝染色观察硬脑膜肥大细胞的数量及脱颗粒百分率,免疫组织化学染色法、免疫蛋白质印迹技术观察硬脑膜中环氧化酶-2(COX-2)的阳性细胞数及蛋白表达.结果假手术组和刺激组颈静脉血中CGRP含量分别为(59.20±11.66)pg/ml和(82.84±16.24)pg/ml(t=-3.34);组胺含量分别为(9.87±0.88)ng/ml和(11.59±1.20)ng/ml(t=-3.27);硬脑膜中肥大细胞数量分别为15.46±2.40和11.63±1.67(t=3.71),脱颗粒百分率分别为14.09%±4.53%、29.10%±9.39%(t=-4.07).两组硬脑膜中PGE2的含量分别为(80.70±10.60)pg/ml和(382.30±20.90)pg/ml(t=-16.674);硬脑膜中COX-2阳性细胞数分别为42.00±18.40和139.00±20.50(t=-7.994),COX-2蛋白表达(吸光度值)分别为19.50±9.20和359.20±21.90(t=-5.190).两组间比较,上述指标差异均有统计学意义(P＜0.05).结论电刺激单侧三叉神经节可诱导硬脑膜肥大细胞脱颗粒及神经源性炎症的产生,相关炎症因子的改变可能是偏头痛疼痛发生的重要病理生理基础.
목적 관찰편두통대서경뇌막비대세포탈과립여신경원성염증상관인자적변화,탐토편두통동통산생적가능궤제.방법 64지SD대서수궤분위자격조(32지)화가수술조(32지).전자격대서단측삼차신경절건립편두통모형,방사면역법측정자격측경정맥혈중강개소기인상관태(CGRP)적함량.매련면역흡부법측정자격측경정맥혈중조알화경뇌막중전렬선소E2(PGE2)적함량,갑분알람염색관찰경뇌막비대세포적수량급탈과립백분솔,면역조직화학염색법、면역단백질인적기술관찰경뇌막중배양화매-2(COX-2)적양성세포수급단백표체.결과 가수술조화자격조경정맥혈중CGRP함량분별위(59.20±11.66)pg/ml화(82.84±16.24)pg/ml(t=-3.34);조알함량분별위(9.87±0.88)ng/ml화(11.59±1.20)ng/ml(t=-3.27);경뇌막중비대세포수량분별위15.46±2.40화11.63±1.67(t=3.71),탈과립백분솔분별위14.09%±4.53%、29.10%±9.39%(t=-4.07).량조경뇌막중PGE2적함량분별위(80.70±10.60)pg/ml화(382.30±20.90)pg/ml(t=-16.674);경뇌막중COX-2양성세포수분별위42.00±18.40화139.00±20.50(t=-7.994),COX-2단백표체(흡광도치)분별위19.50±9.20화359.20±21.90(t=-5.190).량조간비교,상술지표차이균유통계학의의(P＜0.05).결론 전자격단측삼차신경절가유도경뇌막비대세포탈과립급신경원성염증적산생,상관염증인자적개변가능시편두통동통발생적중요병리생리기출.
Objective To observe the changes on the neurogenic inflammation-related factors in the dura mater of the rat model of migraine and investigate the possible mechanism of the pain of migraine.Methods SD rats were randomly divided into stimulation group ( n = 32 ) and sham group ( n = 32 ).Unilateral trigeminal ganglion was stimulated to induce migraine for rats in the stimulation group. Rats in the sham group were subjected to sham surgery. The levels of calcitonin gene-related peptide (CGRP) in the blood of jugular vein in the stimulation side were measured by radioimmunoassay. The levels of histamine in peripheral blood and prostaglandin E2 (PGE2 ) in the dura mater were determined by enzyme-linked immunosorbent assay (ELISA). The number of mast cells and percentage of their degranulation in the dura mater were determined under a microscope after toluidine blue staining. Cyclooxygenase 2 (COX-2)expression in the dura mater was evaluated by immunohistochemical staining and western blot analysis. Results In the stimulation group, the level of CGRP in the ipsilateral jugular vein was (82. 84 ± 16. 24)pg/ml and in the sham group was (59. 20 ±11.66) pg/ml (t = -3.34, P ＜ 0. 05 ). The level of histamine in the ipsilateral jugular vein was ( 11.59 ± 1.20) ng/ml and in the sham group was (9. 87 ±0. 88) ng/ml (t = - 3. 27, P ＜ 0. 05). The number of mast cells in the dura mater decreased from 15.46 ± 2. 40 in the stimulation group to 11.63 ± 1.67 in the sham group ( t = 3.71, P ＜ 0. 05 ). Degranulation of mast cells in the dura mater significantly increased from 14. 09% ±4. 53% in the sham group to 29. 10% ±9. 39% in the stimulation group (t = - 4. 07, P ＜ 0. 05 ). The level of PGE2 in the stimulation group was ( 382. 30 ±20. 90) pg/ml and in the sham group was (80. 70 ± 10. 60) pg/ml (t = - 16. 674, P ＜0. 05). The number of COX-2 positive cells significantly increased from 42. 00 ± 18.40 in the sham group to 139.00 ±20. 50 in the stimulation group (t = -7. 994, P ＜0. 05). Also the COX-2 protein level was elevated from 19. 50 ±9. 20 in the sham group to 359. 20 ±21.90 in the stimulation group (t = -5. 190, P ＜0. 05). Conclusions Electrical stimulation on the unilateral trigeminal ganglion induces neurogenic inflammation in the dura mater. Changes on the neurogenic inflammation-related factors are probably the essential pathophysiological mechanism underlying the pain in migraine.