目的探究Apelin在尾核内对大鼠的痛觉调制作用及其可能的作用机制。方法采用辐射热作为伤害性刺激,以安静状态下大鼠的甩尾潜伏期(TFL)为测痛指标,尾核内注射Apelin、吗啡、纳洛酮等,观察给药90min内Apelin的痛觉调制作用及其对吗啡中枢镇痛作用的影响。检测给药40min后大鼠尾核组织和血浆中cAMP与cGMP水平,探究Apelin在痛觉调制过程中可能的作用机制。结果Apelin有显著的痛敏作用,在10^-4mol/L时作用最显著,给药10min后大鼠痛阈下降[(-9.22±1.26)%],40min后痛阈下降至最低[(-16.95±1.46)%],分别与生理盐水组[(-0.32±1.2)%、(0.17±0.80)%]比较有统计学意义(P〈0.01);大鼠尾核内微量注射吗啡后再注射Apelin,结果表明Apelin能抑制吗啡的中枢镇痛作用(P〈0.01);大鼠尾核内注射Apelin后,尾核cAMP含量为(14.08±2.25)nmol/g,血浆cAMP含量为(19.94±4.43)nmol/L,分别与生理盐水组[(133.05±20.41)nmol/g、(38.66±6.73)nmol/L]比较,有非常显著的统计学意义(P〈0.01)。结论Apelin有中枢痛敏作用,这种痛敏作用可能与阿片系统有某种内在联系并通过细胞内第二信使cAMP发挥效应。
Objective To study the effect and possible mechanism of Apelin in caudate on the pain behavior of rat. Methods Tail flick latency (TFL) of rat was taken as pain threshold and radiant heat as nociceprive stimulus. Microinjeeted Apelin into rat' s caudate to observe the effect of Apefin on modulating of pain in CNS and then to study the interaction between Apelin and morphine in modulation of pain. And the contents of cAMP and eGMP in caudate tissue and blood plasma were detected. Results Compared with control groups, the pain threshold of rat decreased when Apelin was injected into caudate alone. Injected 0.5 μl Apelin of 104 moL/L into rat caudate 10 min later,the pain threshold of rat was reduced ( - 9.22 ±1.26) % and 40 min later ( - 16.95 ±1.46 )% compared with normal saline group ( -0.32 ±1.2 )%, (0.17 ±0.80 )% ), and it had statistical significance (P〈0.01). The contents of cAMP in caudate was (14.08 ±2.25)nmol/g and blood plasma (19.94 ±4.43 ) nmol/L compared with normal saline ( 133.05 ±20.41 ) nmol/g, ( 38.66 ±6.73 ) nmol/L, and they had statistical significance(P〈 0.01 ). Conclusions Apelin can facilitate the pain behavior of rat induced by radiant heat stimulus and consequently plays a hyperalgesia role in CNS. Apelin may have interaction with morphine and display its hyperalgesia effect through the intraceflular second messenger cAMP.