Review Article

Crosstalk between Acupuncture and NF-κB in Inflammatory Diseases

Table 1

Inflammatory diseases could be ameliorated by acupuncture through NF-κB pathways.

DiseaseModelsAcupointsAcupuncture administrationMain resultsReference

AsthmaOVA-induced mouse asthma modelGV14, BL12, BL13MA, 30 mins each day, every other day for 4 weeksAcupuncture attenuated inflammation and inhibited Th17 and the Treg activity[22]
Allergic contact dermatitisDNCB-induced mouse atopic dermatitisLI11MA, 8 daysAcupuncture treatment is effective in alleviating allergic contact dermatitis by reducing proinflammatory cytokines and proteins[28]
DNFB-induced mouse atopic dermatitisST36EA, continuous waves, 2 Hz and 1 mA for 5 min, 2 Hz and 1.5 mA for 5 min, and 2 Hz and 2 mA for 20 min each day, 7 daysEA treatment inhibits NF-κB and AP-1 activation, as well as promotes the negative feedback regulation of IL-33 signaling via targeting miR-155 in mast cells[20]
CAGMNNG-induced CAG rat modelST36, CV12MA, 15 mins each day, 60 daysAcupuncture downregulate NF-κB p65, miR-155, and miR-21 and upregulate miR-146a expression in CAG rats[19]
Cognitive impairmentCerebral I/R-injured rat modelDU20, DU24EA, disperse waves, 1 and 20 Hz, 30 mins each day, 10 daysElectroacupuncture ameliorates cognitive impairment through inhibition of NF-κB-mediated neuronal cell apoptosis[29]
COPDSmoking-induced COPD rat modelST36, BL13EA, alternating waves, 10/50 Hz and 2 mA for 30 mins each day, 7 daysEA treatment can reduce the lung inflammatory response and improve the lung function in COPD[16]
DepressionChronic unpredictable stress rat model of depressionGV20, PC6MA, 10 mins each day, every other day for 4 weeksAcupuncture markedly inhibited the activation of NF-κB in the brain regions[30]
GV20, GV29MA, 20 mins each day, 28 daysThe antidepressant effect of acupuncture is effective and has a multitarget characteristic, which may be related to amino acid metabolism and inflammatory pathways[31]
HIBDHIBD rat modelDU14, DU20EA, 2–100 Hz and 3 mA for 30 mins each day, 14 daysEA against hypoxic-ischemic brain damage in rats via NF-κB/neuronal nitric oxide synthase[32]
Neuropathic painPTX-induced neuropathic pain rat modelST36EA, continuous waves, 10 Hz and 1 mA for 10 mins each day, every other day for 15 daysEA treatment attenuates PTX-induced neuropathic pain via inhibiting spinal glia and the TLR4/NF-κB pathway[33]
Neurodegeneration diseaseTelomerase-deficient miceST36MA or EA, 7 daysEA could specifically ameliorate the spatial learning and memory capability for telomerase-deficient mice through the activation of TrkB and NF-κB than MA[34]
ObesityLeptin deficient miceST36EA, continuous waves, 2 Hz, 0.5 and 1 mA for 10 mins each day, three times weekly for one or two consecutive weeksEA prevents weight gain through modulation of HIF-1α-dependent pathways and inflammatory response in obese adipose tissues[17]
High fat diet-induced obesity rat modelST36, ST40, CV3, CV4EA, continuous waves, 2 Hz and 1 mA for 10 mins each day, three times weekly for 8 weeksEA prevents inflammation through activation of Sirt1[24]
OASurgery-induced OA rabbit modelST35, EX-LE5EA, square waves, 2 Hz and 100 Hz alternating polarity for 30 mins each day, 8 weeksEA treatment may delay cartilage degeneration by downregulating inflammatory factors through the NF-κB signaling pathway[23]
PruritusMorphine-induced pruritus mouse modelLI11, SP10EA, square waves, 2/15 Hz and 2 mA for 30 mins each day, 5 daysEA preconditioning improved pruritus through the TLR2/4-MyD88-NF-κB pathway[25]
RASurgery-induced RA rabbit modeST35, EX-LE5EA, continuous waves, 2 Hz and 2 mA for 30 mins each day, 4 weeksEA can reduce the expression of TLR4, MYD88, and NF-κB, which play an important role in treatment of adjuvant arthritis[35]
StrokeMACo rat modelGV20, GV14EA, amplitude-modulated waves, 5 Hz and 2.7–3.0 mA for 25 mins each day, 6 daysEA subacute phase cerebral I/R injuries by reducing S100B-mediated neurotoxicity[18]
LI11, ST36EA, dilatational waves, 1–20 Hz and 2.7–3.0 mA for 30 mins each day, 3 daysEA improves motor impairment via inhibition of microglia-mediated neuroinflammation in the sensorimotor cortex after ischemic stroke[26]
SAPSodium taurocholate-induced SAP rat modelST25MA or EA, 2–100 Hz and 2 mA, twice after SAP inductionBoth MA and EA might have a therapeutic effect on rats with SAP through inhibition of NF-κB expression and a reduction in the release of proinflammatory cytokines[27]
Traumatic injurySurgical trauma rat modelST36, EX-LE7EA, 2 Hz and 60 Hz alternating polarity for 30 mins, once after surgeryEA inhibits apoptosis of splenic lymphocytes in traumatized rats through modulation of the TNF-α/NF-κB signaling pathway[36]
Feeney’s free fall epidural impact method, TBI rat modelGV20, GV25, GV16, GV15, LI4MA, 15 mins, thriceAcupuncture has a bidirectional regulatory effect on the TLR2/4-NF-κB signaling pathway-related genes TLR2, TLR4, and NF-κB in the TBI rat cortex, promoting their expression in the early stage and inhibiting it in the later stage[37]
VDCMi rat modelST36Verum acupunctureAcupuncture could protect cognitive function against oxidative stress induced by CMi, which is partially associated with suppression of NF-κB-p53 activation[38]

MA: manual acupuncture; EA: electroacupuncture; OVA: ovalbumin; DNCB: 1-chloro-2,4-dini-trobenzene; DNFB: 2,4-dinitrofluorobenzene; CAG: chronic atrophic gastritis; MNNG: N-methyl-N′-nitro-N-nitrosoguanidine; I/R: ischemia/reperfusion; COPD: chronic obstructive pulmonary disease; HIBD: hypoxic-ischemic brain damage; PTX: paclitaxel; OA: osteoarthritis; RA: rheumatoid arthritis; MACo: middle cerebral artery occlusion; SAP: severe acute pancreatitis; TBI: traumatic brain injury; VD: vascular dementia; CMi: cerebral multi-infarction.