4.6 Article

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

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出版社

SPANDIDOS PUBL LTD
DOI: 10.3892/ijmm.2012.1184

关键词

electroacupuncture; Zusanli (ST36) and Quchi (LI11) acupoints; cerebral ischemia/reperfusion; Toll-like receptor 4/nuclear factor-kappa B pathway; inflammatory response

资金

  1. Special Program for Key Basic Research Project of the China Ministry of Science and Technology (973 Program) [2010CB534900]
  2. National Natural Science Foundation of China [30901935]

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Inflammatory response has been shown to play a critical role in brain damage after cerebral ischemia-reperfusion (I/R) injury, which is tightly regulated by the Toll-like receptor (TLR)4/nuclear factor (NF)-kappa B pathway; therefore, suppression of TLR4/NF-kappa B signaling has become a promising target for the anti-inflammatory treatment in ischemic stroke. Acupuncture has been used as a complementary and alternative therapy practice that supplements conventional medicine. Numerous studies 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 evaluated the neuroprotective and anti-inflammatory activities of electroacupuncture at Quchi and Zusanli, and investigated the underlying molecular mechanisms. We found that electroacupuncture at Quchi (LI11) and Zusanli (ST36) acupoints significantly improved the ischemia-associated scores of neurological deficits, reduced cerebral infarction and alleviated inflammatory responses. Moreover, the crucial signaling molecules in the TLR4/NF-kappa B signaling pathway were regulated by acupuncture, which coincided with suppressed secretion levels of inflammatory cytokines such as TNF-alpha, IL-1 beta and IL-6. Our data suggest that electroacupuncture exerts a neuroprotective function in ischemic stroke through inhibition of TLR4/NF-kappa B-mediated inflammation.

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