CAJ | 학술논문

目的：研究神经肽FF （NPFF）对内吗啡肽2（EM-2）在急性痛与炎症痛中镇痛作用的调节。方法雄性昆明系小鼠，体重（20±2） g，侧脑室埋管后，水浴甩尾实验和福尔马林痛实验各随机分为8组，即盐水对照组、EM-2组、NPFF受体拮抗剂RF9组、EM-2+RF9组、低剂量NPFF+EM-2组、中剂量NPFF+EM-2组、高剂量NPFF+EM-2组、高剂量NPFF+RF9+EM-2组，每组8只小鼠。侧脑室注射药物NPFF、EM-2和RF9。小鼠水浴甩尾实验研究NPFF对EM-2中枢镇痛的调节作用，福尔马林痛实验研究NPFF对EM-2急性痛与炎症痛镇痛的调节作用。结果水浴甩尾实验结果显示，EM-27.5 nmol可延长小鼠的甩尾潜伏期， NPFF 5，10，15 nmol可剂量依赖性增强EM-2的镇痛作用。福尔马林痛实验结果显示，EM-215 nmol对第一相急性痛与第二相炎症痛均有镇痛作用， NPFF 10，15，20 nmol可剂量依赖性增强EM-2的镇痛作用。在2个实验中，RF9与NPFF联合给药后，RF9能拮抗NPFF对EM-2镇痛的增强作用。结论在小鼠水浴甩尾实验和福尔马林痛实验中，NPFF通过作用于NPFF受体拮抗剂RF9，剂量依赖性增强EM-2对急性痛和炎症痛的镇痛作用。
목적：연구신경태FF （NPFF）대내마배태2（EM-2）재급성통여염증통중진통작용적조절。방법웅성곤명계소서，체중（20±2） g，측뇌실매관후，수욕솔미실험화복이마림통실험각수궤분위8조，즉염수대조조、EM-2조、NPFF수체길항제RF9조、EM-2+RF9조、저제량NPFF+EM-2조、중제량NPFF+EM-2조、고제량NPFF+EM-2조、고제량NPFF+RF9+EM-2조，매조8지소서。측뇌실주사약물NPFF、EM-2화RF9。소서수욕솔미실험연구NPFF대EM-2중추진통적조절작용，복이마림통실험연구NPFF대EM-2급성통여염증통진통적조절작용。결과수욕솔미실험결과현시，EM-27.5 nmol가연장소서적솔미잠복기， NPFF 5，10，15 nmol가제량의뢰성증강EM-2적진통작용。복이마림통실험결과현시，EM-215 nmol대제일상급성통여제이상염증통균유진통작용， NPFF 10，15，20 nmol가제량의뢰성증강EM-2적진통작용。재2개실험중，RF9여NPFF연합급약후，RF9능길항NPFF대EM-2진통적증강작용。결론재소서수욕솔미실험화복이마림통실험중，NPFF통과작용우NPFF수체길항제RF9，제량의뢰성증강EM-2대급성통화염증통적진통작용。
Objective To investigate the modulation of neuropeptide FF (NPFF) on endomorphin-2 (EM-2) induced antinociception in acute and inflammatory pain. Methods Male Kunming mice weighing (20 ± 2)g (n=128) were divided into eight groups in the mouse tail-immersion test (n=64) and formalin test (n=64), including saline group, EM-2 group, RF9 group (NPFF antagonist), EM-2+RF9 group, low dose NPFF+EM-2 group, medium dose NPFF+EM-2 group, high dose NPFF+EM-2 group, high dose NPFF+RF9+EM-2 group, and each group contains eight mice. Drugs (NPFF, EM-2 and RF9) were injected into the lateral ventricle through the cannula. The mouse tail-immersion test was used to investigate the modulating effects of NPFF on EM-2-induced central antinociception. The mouse Formalin test was used to investigate the modulation of NPFF on EM-2 induced antinociceptive effects in acute and inflammatory pain. Results In the mouse tail-immersion test, NPFF (5, 10, 15 nmol, i.c.v.) dose-dependently enhanced the central antinociception of EM-2 (7.5 nmol, i.c.v.). Furthermore, in the mouse Formalin test, NPFF (10, 15, 20 nmol, i.c.v.) also dose-dependently augmented the antinociceptive effcet caused by intracerebroventricular injection of 15 nmol EM-2 in Forma-lin-induced acute and inflammatory pain. Moreover, these modulating effect of NPFF on EM-2 were marked-ly prevented by pretreatment with NPFF receptors selective antagonist RF9. Conclusion NPFF (i.c.v.) dose-dependently can improve the EM-2-induced central antinociception in acute and inflammatory pain by NPFF receptors.