OBJECTIVE: To evaluate the effect of acupuncture on neuroinflammation in traumatic brain injury(TBI) rats by stimulating Yamen(GV 15), Fengfu(GV16), Baihui(GV 20), Shuigou(GV 26) and Hegu(LI 4)acupoints and to investigate the mechanism underpinning this effect.METHODS: A TBI model was induced in SpragueDawley rats using Feeney's freefall impact method.Acupuncture to stimulate the Yamen(GV 15), Fengfu(GV 16), Baihui(GV 20), Shuigou(GV 26) and Hegu(LI 4) acupoints was performed on the TBI rats. After 3 consecutive days of acupuncture treatment, we investigated signal molecules, receptors and microglia related to neuroinflammation in brain tissue of the TBI rats and analyzed the possi-ble mechanism underlying the effect of acupuncture on neuroinflammation.RESULTS: After the acupuncture treatment, ionized calcium binding adaptor molecule 1(Iba1), a protein specific to microglia, was investigated. In the cortical layer of damaged brain tissue in TBI rats,the Iba1-positive area was 3.3% ± 0.9% in the rats that received acupuncture compared with 5.2% ±1.4% in the TBI rats that did not receive acupuncture, and the microglia were smaller with more slender protrusions in the acupuncture-treated rats.This result indicates that acupuncture can significantly reduce microglia activation in TBI rats. A possible mechanism for this effect is that acupuncture reduces the expression of autotaxin and lysophosphatidic acid. Together, these constitute the autotaxin-lysophosphatidic acid axis, which induces microglial activation in the brains of TBI rats. Acupuncture treatment may downregulate the expression of Lysophosphatidic acid(LPA) receptor(LPAR) 1 and LPAR2 on the microglial cytomembrane, which affects the microglia activation process.CONCLUSION: Acupuncture stimulating the Yamen(GV 15), Fengfu(GV 16), Baihui(GV 20),Shuigou(GV 26) and Hegu(LI 4) acupoints can effectively inhibit the development of neuroinflammation after TBI. One possible mechanism for this effect is that acupuncture downregulates LPA synthesis and affects the LPA-LPAR pathway by inhibiting LPAR1 and LPAR2, thereby inhibiting microglial activation and reducing neuroinflammation.