CAJ | 학술논문

目的探讨电针对大鼠吗啡耐受时脊髓背角细胞外信号调节激酶1/2(ERK1/2)活性的影响.方法取鞘内置管成功的雄性SD大鼠25只,采用随机数字表法,将其分为5组(n=5):生理盐水组(NS组)鞘内注射生理盐水10μl；吗啡组(M组)鞘内注射吗啡10 μg；错义寡核苷酸组(MO组)鞘内注射吗啡10μg+ ERK1/2错义寡核苷酸10μg;反义寡核苷酸组(AO组)鞘内注射吗啡10 μg+ERK1/2反义寡核苷酸10 μg；电针组(EA组)鞘内注射吗啡10 μg,同时每日首次给药后电针大鼠阳陵泉和足三里(频率2 Hz,波宽1 ms,电流强度3 mA,刺激时间30 min).各组注射药物容量均为10μl,2次/d,连续7d.于鞘内给药前、鞘内给药2、4、6d和鞘内给药结束后1 d(T0-4)测定机械痛阈.于T4时机械痛阈测定结束后,取脊髓背角组织,采用Western blot法测定大鼠ERK1/2和磷酸化ERK1/2(p-ERK1/2)的表达.结果 M组、MO组和AO组和EA组发生了吗啡耐受,EA组吗啡耐受程度最轻.与NS组比较,M组和MO组p-ERK1/2表达上调,AO组总ERK1/2表达下调(P＜0.05),EA组上述指标差异无统计学意义(P＞0.05)；与M组和MO组比较,AO组p-ERK1/2和总ERK1/2表达下调,EA组p-ERK1/2表达下调(P＜0.05)；与AO组比较,EA组p-ERK1/2和总ERK1/2表达上调(P＜0.05).结论电针可抑制慢性吗啡给药所导致的脊髓背角ERK1/2活性升高,从而缓解吗啡耐受的形成.
목적 탐토전침대대서마배내수시척수배각세포외신호조절격매1/2(ERK1/2)활성적영향.방법 취초내치관성공적웅성SD대서25지,채용수궤수자표법,장기분위5조(n=5):생리염수조(NS조)초내주사생리염수10μl；마배조(M조)초내주사마배10 μg；착의과핵감산조(MO조)초내주사마배10μg+ ERK1/2착의과핵감산10μg;반의과핵감산조(AO조)초내주사마배10 μg+ERK1/2반의과핵감산10 μg；전침조(EA조)초내주사마배10 μg,동시매일수차급약후전침대서양릉천화족삼리(빈솔2 Hz,파관1 ms,전류강도3 mA,자격시간30 min).각조주사약물용량균위10μl,2차/d,련속7d.우초내급약전、초내급약2、4、6d화초내급약결속후1 d(T0-4)측정궤계통역.우T4시궤계통역측정결속후,취척수배각조직,채용Western blot법측정대서ERK1/2화린산화ERK1/2(p-ERK1/2)적표체.결과 M조、MO조화AO조화EA조발생료마배내수,EA조마배내수정도최경.여NS조비교,M조화MO조p-ERK1/2표체상조,AO조총ERK1/2표체하조(P＜0.05),EA조상술지표차이무통계학의의(P＞0.05)；여M조화MO조비교,AO조p-ERK1/2화총ERK1/2표체하조,EA조p-ERK1/2표체하조(P＜0.05)；여AO조비교,EA조p-ERK1/2화총ERK1/2표체상조(P＜0.05).결론 전침가억제만성마배급약소도치적척수배각ERK1/2활성승고,종이완해마배내수적형성.
Objective To investigate the effect of electroacupuncture (EA) on the activity of extracellular signal-regulated kinase 1/2 (ERK1/2) in the spinal dorsal horn during morphine tolerance in rats.Methods Twenty-five healthy male Sprague-Dawley rats in which intrathecal (IT) catheters were successfully implanted with-out complications were randomly divided into 5 groups (n =5 each):group normal saline (NS) 10 μl IT twice a day × 7 days; group M morphine 10μg (10 μl) IT twice a day × 7 days; group MO morphine 10 μg + missense oligonucleotide (ODN) 10μg (10 μl) twice a day × 7 days; group AO morphine 10 μg + antisense ODN 10 μg (10μl) twice a day×7 days; group EA morphine 10 μg (10μl) twice a day×7 days + EA (frequency 2 Hz,wave length 1 ms,intensity 3 mA).EA of Yanglingquan and Zusanli lasting for 30 min was performed after first IT administration of morphine once a day for 7 days.Mechanical pain threshold (MPT) was measured before IT administration and at day 2,4,6 of IT administration and 1 day after the end of IT administration.The animals were sacrificed after the last MPT measurement,and L3-5 segments of the spinal cord were isolated to detect the expression of ERK1/2 and phosphor-ERK1/2 (p-ERK1/2) in the spinal dorsal horn by Western blot analysis.Results Morphine tolerance developed in groups M,MO and AO,and was lightest in group EA.Compared with group NS,the expression of p-ERK1/2 was significantly up-regulated in groups M and MO,the expression of ERK1/2 was down-regulated in group AO (P ＜ 0.05),and no significant change was found in the indexes mentioned above in group EA (P ＞ 0.05).Compared with groups M and MO,the expression of p-ERK1/2 and ERK1/2 was significantly down-regulated in group AO,and the expression of p-ERK1/2 was down-regulated in group EA (P ＜0.05).Compared with group AO,the expression of p-ERK1/2 and ERK1/2 was significantly up-regulated in group EA (P ＜ 0.05).Conclusion EA can inhibit chronic morphine tolerance-induced increased activity of ERK1/2 in the spinal dorsal horn and alleviate the development of morphine tolerance in rats.