首页> 外文期刊>International journal of molecular medicine >Electroacupuncture exerts anti-inflammatory effects in cerebral ischemia-reperfusion injured rats via suppression of the TLR4/NF-κB pathway
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Electroacupuncture exerts anti-inflammatory effects in cerebral ischemia-reperfusion injured rats via suppression of the TLR4/NF-κB pathway

机译:通过抑制TLR4 / NF-κB途径,电针在脑缺血再灌注大鼠中对脑缺血再灌注大鼠产生抗炎作用

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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)-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.
机译:已经显示出炎症反应在脑缺血再灌注(I / R)损伤后在脑损伤中发挥关键作用,其受到Toll样受体(TLR)4 /核因子(NF)-κB途径紧密调节;因此,抑制TLR4 / NF-κB信号传导已成为缺血性中风中抗炎治疗的有希望的靶标。针灸被用作补充常规药物的互补和替代治疗实践。众多研究表明针灸在中风康复中的临床疗效。然而,其神经保护作用的精确机制仍然明白。使用局灶性脑I / R受损的大鼠模型,在本研究中,我们评估了Quchi和Zusanli电针的神经保护和抗炎活性,并研究了下面的分子机制。我们发现Quchi(Li11)和Zusanli(ST36)穴位的电针显着改善了神经缺陷的缺血相关评分,减少了脑梗死和缓解炎症反应。此外,TLR4 / NF-κB信号传导途径中的关键信号分子由针灸调节,其与抑制炎症细胞因子如TNF-α,IL-1β和IL-6的分泌水平相吻合。我们的数据表明,通过抑制TLR4 / NF-κB介导的炎症,电针在缺血性中风中发挥神经保护功能。

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