Lin Jaung-Geng, Chen Wei-Liang
Graduate Institute of Chinese Medical Science, China Medical University, Taiwan.
Am J Chin Med. 2008;36(4):635-45. doi: 10.1142/S0192415X08006107.
The mechanism of acupuncture analgesia (AA) has been widely explored since the 1970s. Early studies investigated the relationship between acupuncture and endogenous opiates (beta-endorphin, enkephalin, endomorphin and dynorphin). Before the 1990s, most experts agreed on the concept that in normal animal models, lower frequency electroacupuncture (EA) stimulates the release of beta-endorphin, enkephalin and endomorphin, which in turn activates the mu- and delta-opioid receptors, and that higher frequency EA stimulates dynorphin which activates the kappa-opioid receptor. Besides endogenous opiates, our studies have focused on serotonin. The serotoninergic descending inhibitory pathway is suggested to be an important mechanism of acupuncture analgesic, collaborating with endogenous opiates. Many efforts have been made to clarify these mechanisms, but to date no satisfactory consensus has been reached. In the late 1990s, researchers began to focus on the different analgesic effects of EA between normal and hyperalgesic animal models. Published data from these studies imply that normal and hyperalgesic animals respond differently to EA. Results from experiments on the anti-hyperalgesia effect of EA have raised a new issue about the influences of EA on receptors to excitatory amino acid in the spinal cord level. Results from various studies have shown that these receptors play a role in the mechanism of AA. Recently, research on the autonomic nervous system (ANS) seem to indicate its connection with acupuncture. The inflammatory reflex (via the ANS) might be a crucial part of anti-hyperalgesia elicited by acupuncture, and this reflex, which regulates the immune system in the organism, can elucidate not only the mechanism of AA but also the mechanism of acupuncture applied to other inflammatory conditions. Innovation of functional image study enables us to analyze the responses of cortex on living human body to acupuncture. However, results of these experiments are still controversial. After 30 years of acupuncture research, there are still many puzzles left to be solved regarding the mechanism of AA.
自20世纪70年代以来,针刺镇痛(AA)的机制一直受到广泛探索。早期研究调查了针刺与内源性阿片类物质(β-内啡肽、脑啡肽、内吗啡肽和强啡肽)之间的关系。在20世纪90年代之前,大多数专家认同这样的概念:在正常动物模型中,低频电针(EA)刺激β-内啡肽、脑啡肽和内吗啡肽的释放,进而激活μ-和δ-阿片受体;而高频EA刺激强啡肽,其激活κ-阿片受体。除了内源性阿片类物质,我们的研究聚焦于5-羟色胺。5-羟色胺能下行抑制通路被认为是针刺镇痛的重要机制,与内源性阿片类物质协同作用。人们为阐明这些机制付出了诸多努力,但迄今为止尚未达成令人满意的共识。在20世纪90年代后期,研究人员开始关注正常和痛觉过敏动物模型中EA的不同镇痛效果。这些研究发表的数据表明,正常和痛觉过敏动物对EA的反应不同。EA抗痛觉过敏作用的实验结果引发了一个关于EA对脊髓水平兴奋性氨基酸受体影响的新问题。各种研究结果表明,这些受体在AA机制中发挥作用。最近,对自主神经系统(ANS)的研究似乎表明其与针刺有关。(通过ANS的)炎症反射可能是针刺引起抗痛觉过敏的关键部分,并且这种调节机体免疫系统的反射不仅可以阐明AA的机制,还能解释针刺应用于其他炎症性疾病的机制。功能影像研究的创新使我们能够分析活体人体皮层对针刺的反应。然而,这些实验结果仍存在争议。经过30年的针刺研究,关于AA机制仍有许多谜题有待解决。