College of Rehabilitation Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350122, PR China.
Int J Mol Med. 2013 Jan;31(1):75-80. doi: 10.3892/ijmm.2012.1184. Epub 2012 Nov 16.
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)-κB pathway; therefore, suppression of TLR4/NF-κB 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-κB signaling pathway were regulated by acupuncture, which coincided with suppressed secretion levels of inflammatory cytokines such as TNF-α, IL-1β and IL-6. Our data suggest that electroacupuncture exerts a neuroprotective function in ischemic stroke through inhibition of TLR4/NF-κB-mediated inflammation.
炎症反应在脑缺血再灌注(I/R)损伤后脑损伤中起着关键作用,其受到 Toll 样受体(TLR)4/核因子(NF)-κB 途径的严格调控;因此,抑制 TLR4/NF-κB 信号转导已成为缺血性中风抗炎治疗的有前途的靶点。针灸作为一种补充和替代传统医学的治疗方法已经得到广泛应用。大量研究表明针灸在中风康复中的临床疗效。然而,其神经保护作用的确切机制仍知之甚少。本研究采用局灶性脑 I/R 损伤大鼠模型,评估了曲池和足三里电针对缺血性损伤的神经保护和抗炎作用,并探讨了其潜在的分子机制。我们发现,针刺曲池(LI11)和足三里(ST36)穴可显著改善与缺血相关的神经功能缺损评分,减少脑梗死,并减轻炎症反应。此外,TLR4/NF-κB 信号通路中的关键信号分子也受到针刺的调节,同时炎症细胞因子如 TNF-α、IL-1β 和 IL-6 的分泌水平也受到抑制。我们的数据表明,电针对缺血性中风具有神经保护作用,其机制可能与抑制 TLR4/NF-κB 介导的炎症反应有关。