肝臟缺血再灌注損傷 α7nAChR 阿托品 迷走神經(jīng)論文

1、肝臟缺血再灌注損傷論文：阿托品減輕肝臟缺血再灌注損傷的7nAChR機(jī)制【中文摘要】肝臟缺血再灌注損傷(hepatic ischemia-reperfusion injury,HIRI)是肝臟外科常見的病理生理過程,臨床工作中如嚴(yán)重肝外傷、肝切除、肝移植等均涉及這一過程。缺血再灌注損傷機(jī)制是復(fù)雜的,涉及細(xì)胞凋亡和壞死等途徑。人類不同原因致肝臟損傷,甚至肝臟纖維化過程中凋亡是一個(gè)重要的特征。研究表明在缺血再灌注引起的肝損傷過程中存在肝細(xì)胞凋亡。尼古丁7受體(7-nicotinic acetylcholine receptor,7nAChR)在機(jī)體廣泛存在,包括神經(jīng)元細(xì)胞、免疫細(xì)胞、內(nèi)皮細(xì)胞和上皮細(xì)

2、胞等。7nAChR是一個(gè)重要的炎癥調(diào)節(jié)受體,在膽堿能抗炎通路介導(dǎo)的神經(jīng)-免疫調(diào)節(jié)過程具有重要的作用。膽堿能抗炎通路的核心內(nèi)容是:迷走神經(jīng)釋放的主要遞質(zhì)乙酰膽堿可以激活巨噬細(xì)胞膜上7nAChR,有效減少巨噬細(xì)胞釋放致炎細(xì)胞因子和調(diào)節(jié)抗炎細(xì)胞因子含量,從而達(dá)到控制炎癥反應(yīng)程度,發(fā)揮抗炎癥損傷、感染和休克作用。我們的研究發(fā)現(xiàn)高血壓時(shí)膽堿能抗炎通路功能下降,7nAChR表達(dá)量減少,7nAChR(-/-)致高血壓器官損傷加重,7nAChR選擇性激動劑治療自發(fā)性高血壓大鼠可以減輕其器官損.【英文摘要】Hepatic ischemia-reperfusion injury occurs in a numbe

3、r of clinical settings,including hemorrhagic shock,and liver surgery.The mechanism of liver injury remains far from full explanation.There is no single factor responsible for liver injury after its temporary ischemia and reperfusion. Apoptosis plays an important role in many diseases, such as hepati

4、c fibrosis-renal tubular ectasia syndrome and hepatic ischemia reperfusion.7 nicotinic acetylcholine receptor (7nAChR) is widely expressed in neuronal an.【關(guān)鍵詞】肝臟缺血再灌注損傷 7nAChR 阿托品 迷走神經(jīng)【英文關(guān)鍵詞】hepatic ischemia reperfusion injury 7nAChR atropine hepatic vagus nerve【目錄】阿托品減輕肝臟缺血再灌注損傷的7nAChR機(jī)制中文摘要5-8英文摘要8-9中英文縮寫詞表10-12前言12-16實(shí)驗(yàn)材料16-23實(shí)驗(yàn)方法23-32實(shí)驗(yàn)結(jié)果32-44討論44-47結(jié)