Pain is a widespread and complex symptom which causes serious emotional and social burdens to individuals and society. Most patients with pain rely heavily on over the counter (OTC) and prescription pain killers. However, there would be a number of issues that arise from the use of pain killers, in which safety and addiction are the most critical issues. For traditional Chinese medicine (TCM), pain is a result of the meridians being blocked. This could occur as a symptom of or be caused by various diseases. In this case, the key to relieve pain depends on dredging the meridian or meridians. Acupuncture has been practiced in China for over 2000 years to lessen pain. It is based on the “meridian theory”. Acupuncture is being used more widely and with a growing number of people in the treatment of pain because it is safer and has fewer side effects. Along with growing use and interest in acupuncture to treat pain, more attention has been paid to the mechanism underlying its analgesic effect, which is mainly associated with the changes of neurotransmitters. In this review, we summarize and analyze the range and mechanism of acupuncture analgesia treatment.

ChiCTR-OOC-14005617; ChiCTR-OOC-15005882.

BACKGROUND Electroacupuncture (EA) at ST36 can significantly improve gastrointestinal symptoms, especially in promoting gastrointestinal motility. The automatic nervous system plays a main role in EA, but few studies exist on how vagovagal and sympathetic reflexes affect EA to regulate gastrointestinal motility. AIM To study the role of vagovagal and sympathetic reflexes in EA at ST36, as well as the associated receptor subtypes that are involved. METHODS Gastric motility was measured with a manometric balloon placed in the gastric antrum area in anesthetized animals. The peripheral nervous discharge was measured using a platinum electrode hooking the vagus or greater splanchnic nerve, and the central nervous discharge was measured with a glass microelectrode in the dorsal motor nucleus of the vagus (DMV). The effects and mechanisms of EA at ST36 were explored in male Sprague-Dawley rats which were divided in to a control group, vagotomy group, sympathectomy group, and microinjection group [including an artificial cerebrospinal fluid group, glutamate (L-Glu) group, and γ-aminobutyric acid (GABA) group] and in genetically modified male mice [β1β2 receptor-knockout (β1β2 -/- ) mice, M2M3 receptor-knockout (M2M3 -/- ) mice, and wild-type control mice]. RESULTS EA at ST36 promoted gastric motility during 30-120 s. During EA, both vagus and sympathetic nerve discharges increased, with a much higher frequency of vagus nerve discharge than sympathetic discharge. The gastric motility mediated by EA at ST36 was interdicted by vagotomy. However, gastric motility mediated by EA at ST36 was increased during 0-120 s by sympathectomy, which eliminated the delay effect of EA during 0-30 s, but it was lower than the control group during 30-120 s. Using gene knockout mice and their wild-type controls to explore the receptor mechanisms, we found that EA at ST36 decreased gastric motility in M2/3 -/- mice, and promoted gastric motility in β1/2 -/- mice. Extracellular recordings showed that EA at ST36 increased spikes of the DMV. Microinjection of L-Glu into the DMV increased gastric motility, while EA at ST36 decreased gastric motility during 0-60 s, and promoted gastric motility during 60-120 s. Injection of GABA reduced or increased gastric motility, and reduced the promoting gastric motility effect of EA at ST36. CONCLUSION These data suggest that EA at ST36 modulates gastric motility via vagovagal and sympathetic reflexes mediated through M2/3 and β1/2 receptors, respectively. Sympathetic nerve activity mediated through β1/2 receptors is associated with an early delay in modulation of gastric motility by EA at ST36.

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There is evidence to show that electro-acupuncture (EA) has a promotive effect on both lipolysis and thermogenesis, and that these mechanisms underlie the anti-obesity effect of EA. The sympathetic nervous system (SNS) is known to play a role in thermogenesis. Additionally, obesity is characterized by a chronic low-grade inflammatory state. Based on these findings, the aim of the present study is to investigate the potential neuro-immune mechanisms underlying the therapeutic effect of EA in obesity. In the experiment, we used a high fat diet (HFD) rats model to study the effect of EA in reducing body weight. EA increases the activity of sympathetic nerves in inguinal white adipose tissue (iWAT), especially in the HFD group. Compared to HFD rats, EA can decrease sympathetic associated macrophage (SAM) and the level of norepinephrine transporter protein (Slc6a2). The relative uncoupling protein 1 expression shows EA increases thermogenesis in iWAT, and increases β3 receptors. Interestingly, injecting β antagonist in iWAT increases Slc6a2 protein levels. Additionally, the SNS-macrophage cross-talk response to EA showed in iWAT but not in epididymis white adipose tissue. The results of the present study indicate that EA exerts its anti-obesity effect via three mechanisms: (1) inhibition of SAMs and the norepinephrine transporter protein SlC6a2, (2) promoting SNS activity and thermogenesis, and (3) regulating immunologic balance.