中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2010年
8期
962-965
,共4页
药物耐受性%吗啡%炎症%电针%降钙素基因相关肽%P物质%脑源性神经营养因子
藥物耐受性%嗎啡%炎癥%電針%降鈣素基因相關肽%P物質%腦源性神經營養因子
약물내수성%마배%염증%전침%강개소기인상관태%P물질%뇌원성신경영양인자
Drug tolerance%Morphine%Inflammation%Electroacupuncture%Calcitonin gene-related peptide%Substance P%Brain-derived neurotrophic factor
目的 探讨炎性痛-吗啡耐受大鼠背根神经节降钙素基因相关肽(CGRP)、P物质(SP)及脑源性神经营养因子(BDNF)表达的变化及电针对吗啡耐受的影响.方法 取鞘内置管成功的25只大鼠,于左后足踝关节腔注射完全弗氏佐剂50μl致炎,致炎后第4天开始鞘内给药.随机分为5组(n=5):A组鞘内给予生理盐水10μl,2次/d,连续7 d;B组鞘内给予吗啡10 μg/kg(10μl),2次/d,仅给药1 d;C组鞘内给予吗啡10 μg/kg(10μl),2次/d,连续7 d;D组鞘内给药方法同C组,同时每日首次给药后用电针刺激仪电针大鼠阳陵泉穴和足三里穴,刺激强度2 mA,刺激频率2 Hz,波宽0.6ms,刺激时间30 min;E组电针刺激频率15Hz,波宽0.4 m,余同D组.于致炎前、鞘内给药前1 d、给药后1、2、3、4、5、6、7 d(T0-8)时测定大鼠后肢热缩足潜伏期(PWL).给药7 d后取L4～L6背根神经节,采用RT-PCR法测定CGRP、SP、BDNF的mRNA表达.结果 与T0时比较,各组T1时PWL缩短(P＜0.05);与T1时比较,B组～E组T2时PWL延长(P＜0.05);与T2时比较,B组～E组T3-8时PWL缩短(P＜0.05).与A组比较,B组～E组PWL延长,C组CGRP mRNA、SP mRNA、BDNF mRNA表达上调(P＜0.05);与B组比较,C组～E组PWL延长(P＜0.05);与C组比较,D组和E组PWL延长,CGRP mRNA、SP mRNA、BDNF mRNA表达下调(P＜0.05);与D组比较,E组PWL缩短,CGRP mRNA、SPmRNA、BDNF mRNA表达上调(P＜0.05).结论 大鼠背根神经节内CGRP mRNA、SPmRNA、BDNF mRNA表达上调参与了吗啡镇痛耐受的形成;电针治疗可抑制吗啡镇痛耐受的形成,机制可能与抑制背根神经节内CGRP mRNA、SP mRNA、BDNF mRNA表达有关.
目的 探討炎性痛-嗎啡耐受大鼠揹根神經節降鈣素基因相關肽(CGRP)、P物質(SP)及腦源性神經營養因子(BDNF)錶達的變化及電針對嗎啡耐受的影響.方法 取鞘內置管成功的25隻大鼠,于左後足踝關節腔註射完全弗氏佐劑50μl緻炎,緻炎後第4天開始鞘內給藥.隨機分為5組(n=5):A組鞘內給予生理鹽水10μl,2次/d,連續7 d;B組鞘內給予嗎啡10 μg/kg(10μl),2次/d,僅給藥1 d;C組鞘內給予嗎啡10 μg/kg(10μl),2次/d,連續7 d;D組鞘內給藥方法同C組,同時每日首次給藥後用電針刺激儀電針大鼠暘陵泉穴和足三裏穴,刺激彊度2 mA,刺激頻率2 Hz,波寬0.6ms,刺激時間30 min;E組電針刺激頻率15Hz,波寬0.4 m,餘同D組.于緻炎前、鞘內給藥前1 d、給藥後1、2、3、4、5、6、7 d(T0-8)時測定大鼠後肢熱縮足潛伏期(PWL).給藥7 d後取L4～L6揹根神經節,採用RT-PCR法測定CGRP、SP、BDNF的mRNA錶達.結果 與T0時比較,各組T1時PWL縮短(P＜0.05);與T1時比較,B組～E組T2時PWL延長(P＜0.05);與T2時比較,B組～E組T3-8時PWL縮短(P＜0.05).與A組比較,B組～E組PWL延長,C組CGRP mRNA、SP mRNA、BDNF mRNA錶達上調(P＜0.05);與B組比較,C組～E組PWL延長(P＜0.05);與C組比較,D組和E組PWL延長,CGRP mRNA、SP mRNA、BDNF mRNA錶達下調(P＜0.05);與D組比較,E組PWL縮短,CGRP mRNA、SPmRNA、BDNF mRNA錶達上調(P＜0.05).結論 大鼠揹根神經節內CGRP mRNA、SPmRNA、BDNF mRNA錶達上調參與瞭嗎啡鎮痛耐受的形成;電針治療可抑製嗎啡鎮痛耐受的形成,機製可能與抑製揹根神經節內CGRP mRNA、SP mRNA、BDNF mRNA錶達有關.
목적 탐토염성통-마배내수대서배근신경절강개소기인상관태(CGRP)、P물질(SP)급뇌원성신경영양인자(BDNF)표체적변화급전침대마배내수적영향.방법 취초내치관성공적25지대서,우좌후족과관절강주사완전불씨좌제50μl치염,치염후제4천개시초내급약.수궤분위5조(n=5):A조초내급여생리염수10μl,2차/d,련속7 d;B조초내급여마배10 μg/kg(10μl),2차/d,부급약1 d;C조초내급여마배10 μg/kg(10μl),2차/d,련속7 d;D조초내급약방법동C조,동시매일수차급약후용전침자격의전침대서양릉천혈화족삼리혈,자격강도2 mA,자격빈솔2 Hz,파관0.6ms,자격시간30 min;E조전침자격빈솔15Hz,파관0.4 m,여동D조.우치염전、초내급약전1 d、급약후1、2、3、4、5、6、7 d(T0-8)시측정대서후지열축족잠복기(PWL).급약7 d후취L4～L6배근신경절,채용RT-PCR법측정CGRP、SP、BDNF적mRNA표체.결과 여T0시비교,각조T1시PWL축단(P＜0.05);여T1시비교,B조～E조T2시PWL연장(P＜0.05);여T2시비교,B조～E조T3-8시PWL축단(P＜0.05).여A조비교,B조～E조PWL연장,C조CGRP mRNA、SP mRNA、BDNF mRNA표체상조(P＜0.05);여B조비교,C조～E조PWL연장(P＜0.05);여C조비교,D조화E조PWL연장,CGRP mRNA、SP mRNA、BDNF mRNA표체하조(P＜0.05);여D조비교,E조PWL축단,CGRP mRNA、SPmRNA、BDNF mRNA표체상조(P＜0.05).결론 대서배근신경절내CGRP mRNA、SPmRNA、BDNF mRNA표체상조삼여료마배진통내수적형성;전침치료가억제마배진통내수적형성,궤제가능여억제배근신경절내CGRP mRNA、SP mRNA、BDNF mRNA표체유관.
Objective To investigate the changes in the expression of calcitonin gene-related peptide (CGRP), substance P (SP) and brain-derived neurotrophic factor (BDNF) in dorsal root ganglion (DRG) and the effect of electroacupuncture (EA) on morphine tolerance in rats with chronic inflammatory pain (CIP) and morphine tolerance. Methods Twenty-five 8-month-old male SD rats weighing 230-250 g in which intrathecal (IT)catheters were successfully implanted without complications were randomly divided into 5 groups ( n = 5 each):groupA CIP + normal saline (NS) 10 μl IT twice a day for 7 consecutive days; group B CIP + morphine 10 μg/kg ( 10 μl) IT twice for the first day only; group C CIP + morphine 10 μg/kg ( 10 μl) IT twice a day for 7 consecutive days; group D CIP + EA (intensity 2 mA, frequency 2 Hz, wave length 0.6 ms) + morphine 10 μ g/kg (10 μl) IT twice a day for7 consecutive days; group E CIP + EA (intensity 2 mA, frequency 15 Hz,wave length 0.4 ms) + morphine 10μg/kg (10 μl) IT twice a day for7 consecutive days. CIP was induced by injecting complete Freund's adjuvant (CFA) into the ankle joint of the left hindlimb. IT morphine or NS was started on the 4th day after induction of CIP. EA of Yanglingquan and Zusanli lasting 30 min was performed once a day after first IT administration of morphine for 7 days. Paw withdrawal latency (PWL) to a thermal nociceptive stimulus was measured before induction of CIP, 1 day before (baseline) and at day 1-7 after administration (T0-8) . The animals were sacrificed after the last PWL measurement. The DRGs of the lumbar segment (L4-6) were removed for determination of CGRP, SP and BDNF mRNA expression using RT-PCR. Results PWL was significantly shorter at T1 than at T0 in all groups, and at T3-8 than at T2 in group B-E, while longer at T2 than at T1 in group B-E ( P ＜0.05). PWL was significantly longer in group B-E and CGRP, SP and BDNF mRNA expression higher in group C than in group A ( P ＜ 0.05). PWL was significantly longer in group C-E than in group B ( P ＜ 0.05). PWL was significantly longer and CGRP, SP and BDNF mRNA expression lower in group D and E than in group C ( P ＜0.05). PWL was significantly lower and CGRP, SP and BDNF mRNA expression higher in group E than in group D ( P ＜ 0.05). Conclusion Up-regulation of the expression of CGRP, SP and BDNF mRNA in DRG is involved in the devepopment of morphine tolerance. EA can inhibit the devepopment of morphine tolerance by inhibiting the expression of CGRP2 SP and BDNF mRNA.
