Pavlov Valentin A
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research 350 Community Drive, Manhasset, NY 11030, USA.
Int J Clin Exp Med. 2008;1(3):203-12. Epub 2008 Jun 5.
Recent studies have demonstrated that cytokine levels and inflammation can be regulated by specifically augmenting cholinergic signaling via the efferent vagus nerve and the alpha7 subunit-containing nicotinic acetylcholine receptor (alpha7nAChR). Cholinergic modalities, acting through vagus nerve- and/or alpha7nAChR-mediated mechanisms have been shown to suppress excessive inflammation in several experimental models of disease, including endotoxemic shock, sepsis, ischemia-reperfusion injury, hemorrhagic shock, colitis, postoperative ileus and pancreatitis. These studies have advanced the current understanding of the mechanisms regulating inflammation. They have also provided a rationale for exploring new possibilities to treat excessive, disease-underlying inflammation by applying selective cholinergic modalities in preclinical and clinical settings. An overview of this research is presented here.
最近的研究表明，通过传出迷走神经和含α7亚基的烟碱型乙酰胆碱受体（α7nAChR）特异性增强胆碱能信号传导，可以调节细胞因子水平和炎症反应。在包括内毒素性休克、脓毒症、缺血-再灌注损伤、失血性休克、结肠炎、术后肠梗阻和胰腺炎在内的几种疾病实验模型中，通过迷走神经和/或α7nAChR介导机制起作用的胆碱能方式已被证明可抑制过度炎症反应。这些研究推进了目前对炎症调节机制的理解。它们还为在临床前和临床环境中应用选择性胆碱能方式治疗过度的、疾病潜在的炎症反应探索新可能性提供了理论依据。本文对此研究进行概述。
