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Inflammatory response has been shown to play a critical role in brain damageafter cerebral ischemia-reperfusion (I/R) injury, which is tightly regulated bythe Toll-like receptor (TLR)4/nuclear factor (NF)-κB pathway; therefore, suppressionof TLR4/NF-κB signaling has become a promising target for the anti-inflammatorytreatment in ischemic stroke. Acupuncture has been used as a complementary andalternative therapy practice that supplements conventional medicine. Numerousstudies have demonstrated the clinical efficacy of acupuncture in stroke rehabilitation.However, the precise mechanism of its neuroprotective effect remains poorly understood.Using a focal cerebral I/R injured rat model, in the present study we evaluatedthe neuroprotective and anti-inflammatory activities of electroacupuncture atQuchi and Zusanli, and investigated the underlying molecular mechanisms. We foundthat electroacupuncture at Quchi (LI11) and Zusanli (ST36) acupoints significantlyimproved the ischemia-associated scores of neurological deficits, reduced cerebralinfarction and alleviated inflammatory responses. Moreover, the crucial signalingmolecules in the TLR4/NF-κB signaling pathway were regulated by acupuncture, whichcoincided with suppressed secretion levels of inflammatory cytokines such as TNF-α,IL-1β and IL-6. Our data suggest that electroacupuncture exerts a neuroprotectivefunction in ischemic stroke through inhibition of TLR4/NF-κB-mediated inflammation.

Electroacupuncture exerts anti-inflammatory effects in cerebral ischemia-reperfusion injured rats via suppression of the TLR4/NF-κB pathway