Table 2.
The effect of acupuncture on inflammatory and neuropathic pain.
| Study | Model | Intervention | Acupoints | Evaluation | Result |
|---|---|---|---|---|---|
| Hsu et al., (2014) [173] | SD rats | CCI-induced neuropathic pain; EA, 2- and 15-Hz, 20 min | Ipsilateral ST36-ST37 of the affected limb | Behavioral responses to stimuli; expression of TRPV1/4 in the cerebral cortex and lumbar spinal cord | EA relieved neuropathic pain; downregulation of cerebral TRPV4 expression. |
| Jiang et al., (2018) [174] | SD rats | CCI-induced neuropathic pain; EA, 2- and 15-Hz, 20 min | Bilateral L4-L6 Hua Tuo Jia Ji (EX-B2) | GABAA, A1R, TRPV1/4, and mGluR3 in the DRG | EA reduced the pain response, upregulating the GABAA receptor in the spinal cord. |
| Huang et al., (2019) [175] | SD rats | CCI-induced neuropathic pain; EA, 2-, 15- and 50-Hz, 20 min | GV20, GV14 | Expression of the GABAA receptor and the level of glutamate in the hippocampus and periaqueductal gray (PAG) area. | EA reduced the pain response; suppressed hippocampal GABAA receptors; decreased thalamic glutamate levels. |
| Lin et al., (2002) [176] | Human | Preoperative EA, 2- (low) or 100- (high) Hz, 20 min | Bilateral ST36 | Postoperative pain and opioid-related side effects | Both low- and high-frequency EA reduced postoperative analgesic requirements and associated side effects. |
| Wang et al., (1997) [177] | Human | Postoperative TAES, 2- (low) or 100- (high) Hz, 30 min | Bilateral LI4 | Postoperative pain and opioid-related side effects | Both low- and high-frequency EA reduced postoperative analgesic requirements and associated side effects. |
| Chen et al. (2011) [178] | CD1 mice | EA, 2-Hz, 20 min | Bilateral ST36 | Behavioral responses in the paw and ASIC3 overexpression in DRG neurons. | Rescued mechanical hyperalgesia and an ASIC3 downregulation. |
| Chen et al. (2012) [179] | ICR mice | EA, 2-Hz, 15 min | Bilateral ST36 | Behavioral responses in the paw and TRPV1/4 overexpression in DRG neurons. | TRPV1 and TRPV4 upregulation in DRG neurons was attenuated by EA. |
| Huang et al. (2013) [180] | ICR mice | EA, 2-Hz, 15 min | Bilateral ST36 | Behavioral responses in the paw and the overexpression of Nav1 in DRG neurons. | EA attenuated inflammatory pain by suppressing Nav1 overexpression. |
| Wu et al. (2014) [181] | ICR mice | MA, 60 min | Ipsilateral ST36 of the inflamed limb | Behavioral responses in paw; the overexpression of TRPV1/4, ASIC3, and CWP components in the anatomical layers of ST36. | MA induced analgesia, with high TRPV1 and CWP overexpression at ST36 upon MA. |
| Lu et al. (2016) [182] | C57/B6 mice | EA, 2-Hz, 15 min | Ipsilateral and contralateral ST36-ST37 of the inflamed limb | Behavioral responses in the paw; Nav and TRPV1 overexpression in DRG neurons. | Hyperalgesia was suppressed through ipsilateral and contralateral EA. Nav and TRPV1 were suppressed through EA. |
| Liao et al. (2017) [143] | C57/B6 mice | EA, 2-Hz, 15 min | Bilateral ST36 | Behavioral responses in the paw and the expression of Nav, GFAP, Iba-1, S100B, RAGE, and TRPV1 in DRG neurons. | EA attenuated inflammatory pain by suppressing Nav1.8 through S100B, TRPV1, opioid, and adenosine pathways. |
| Liao et al. (2017) [183] | C57/B6 mice | EA, 2-Hz, 15 min | Bilateral ST36 | Behavioral responses in the paw and the expression of GFAP, S100B, RAGE, PKCε, ERK, NF-κB, and COX-2 in DRG neurons. | EA attenuated inflammatory pain by suppressing opioid and adenosine pathways. |
| Yang et al. (2017) [184] | C57/B6 mice | EA, 2-Hz, 15 min | Bilateral ST36 | Behavioral responses in the paw and the expression of TRPV1, PKA, PKC, PI3K, ERK1/2, p38, JNK, Akt, mTOR, CREB, NF-κB, Nav1.7/1.8, GFAP, S100B, and RAGE in DRG neurons. | EA significantly reduced chronic inflammatory pain by downregulating the TRPV1 pathway from the peripheral DRG neurons to the central spinal cord. |
| Yen et al. (2019) [185] | C57/B6 mice | EA, 2-Hz, 15 min | Bilateral LI4 | Behavioral responses in the paw and the expression of TRPV1 and ERK1/2 in the prefrontal cortex, the hypothalamus, the PAG area, and DRG neurons. | Pain alleviation immediately after EA; the expression of TRPV1-associated molecules was attenuated by EA in the prefrontal cortex, the hypothalamus, the PAG area, and DRG. |
| Hsu et al. (2019) [186] | C57/B6 mice | EA, 2-Hz, 15 min | Bilateral ST36 | Behavioral responses in the paw and the expression of TLR2, PI3K, ERK1/2, p38, JNK, Akt, mTOR, CREB, NF-κB, and Nav1.7/1.8 in the thalamus. | EA attenuated inflammatory pain via TLR2 signaling. |
| Yang et al. (2009) [187] | Patients with CTS | MA, 30 min/session, 2 session a week, 8 session in total | Affected side(s), PC6, PC7 | Motor and sensory NCS; designed symptomatic questionnaire. | Short-term acupuncture was as effective as short-term low-dose steroid for mild-to-moderate CTS. |
| Yang et al. (2011) [188] | Patients with CTS | MA, 30 min/session, 2 session a week, 8 session in total | Affected side(s), PC6, PC7 | NCS; global symptom score. | Acupuncture had superior efficacy to steroid treatment not only in terms of objective changes in nerve conduction but also in terms of subjective symptom assessment in long-term follow-up. |
| Yang et al. (2011) [189] | Patients with chronic migraine (CM) | MA, 30 min/session, 2 session a week, 24 session in total | Bilateral BL2, GB20, EX-HN5, EX-HN3 (acupoints relate to the trigeminal and cervical dermatomes) | Changes in headache events, MIDAS scores, HADS scores, BDI-II scores, reduction of medication. | Acupuncture was similarly effective or more effective than prophylactic drug treatment with less side effects in migraine. |
A1R: adenosine A1 receptor; ASIC3: acid-sensing ion channel; BDI-II: Beck Depression Inventory-II; CCI: chronic constriction injury; CWP components: components of calcium wave propagation, including pannexin 1, connexin 43, P2Y1, and P2Y2, which can activate a release of ATP after mechanical stimulation of nonneural cells such as subepithelial fibroblasts; GABAA: γ-aminobutyric acid A; GFAP: glial fibrillary acidic protein, an astrocytic marker; HADS: hospital anxiety and depression scale; Iba-1: ionized calcium-binding adaptor molecule 1, a microglia/macrophage specific protein (marker); MA: manual acupuncture; MIDAS: Migraine Disability Assessment; mGluR3: metabotropic glutamate receptor 3; Navs: voltage-gated sodium channels; NCS: nerve conduction study; RAGE: receptor for advanced glycation end-products; TAES: transcutaneous acupoint electrical stimulation; 100B: calcium-binding protein B.