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迷走神經(jīng)電刺激對(duì)內(nèi)毒素血癥小鼠腸道上皮細(xì)胞緊密連接及肺的血?dú)馄琳系挠绊?/H1>
發(fā)布時(shí)間:2018-03-16 07:18

  本文選題:內(nèi)毒素血癥 切入點(diǎn):迷走神經(jīng)電刺激 出處:《廣東醫(yī)學(xué)》2017年16期  論文類(lèi)型:期刊論文


【摘要】:目的探討迷走神經(jīng)電刺激活化膽堿能抗炎通路對(duì)內(nèi)毒素血癥小鼠的腸道上皮細(xì)胞緊密連接及肺的血?dú)馄琳系谋Wo(hù)作用及其可能機(jī)制。方法雄性Balb/c小鼠腹腔注射脂多糖10 mg/kg,復(fù)制內(nèi)毒素血癥模型。將小鼠隨機(jī)分為4組:(1)假手術(shù)組,暴露分離迷走神經(jīng)但不給予電刺激,給予生理鹽水0.25 m L腹腔注射;(2)內(nèi)毒素血癥組,暴露分離迷走神經(jīng)但不給予電刺激,給予腹腔注射脂多糖10 mg/kg;(3)迷走神經(jīng)電刺激組,在脂多糖腹腔注射后,用5%的戊巴比妥鈉腹腔注射麻醉,暴露分離右側(cè)迷走神經(jīng),連接迷走神經(jīng)電刺激儀刺激右側(cè)迷走神經(jīng)10 min;(4)α-銀環(huán)蛇毒素(α-BGT)組,在迷走神經(jīng)電刺激前20 min皮下給予α-BGT 0.5μg/只,余操作同迷走神經(jīng)電刺激組。在給予脂多糖腹腔注射12 h后采集小鼠的回腸及肺組織標(biāo)本。結(jié)果內(nèi)毒素血癥組、α-BGT組右旋糖酐(FITC-Dextran)水平均高于假手術(shù)組,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。內(nèi)毒素血癥組、α-BGT組FITC-Dextran水平均高于迷走神經(jīng)電刺激組,差異有統(tǒng)計(jì)學(xué)意義(P0.05)。內(nèi)毒素血癥組肺組織occludin水平低于假手術(shù)組,腸道組織occludin水平低于假手術(shù)組、NF-κB水平高于假手術(shù)組(P0.05);α-BGT組occludin水平低于假手術(shù)組,NF-κB水平高于假手術(shù)組(P0.05),腸道組織occludin水平低于假手術(shù)組、NF-κB水平高于假手術(shù)組(P0.05);迷走神經(jīng)電刺激組肺組織occludin水平高于內(nèi)毒素血癥組和α-BGT組,NF-κB水平低于LPS組和α-BGT組,腸道組織occludin水平高于內(nèi)毒素血癥組和α-BGT組,NF-κB水平低于LPS組和α-BGT組(P0.05)。結(jié)論迷走神經(jīng)電刺激活化膽堿能抗炎通路對(duì)內(nèi)毒素血癥小鼠腸道上皮和肺的血?dú)馄琳系耐ㄍ感缘谋Wo(hù)是通過(guò)煙堿型乙酰膽堿受體α7亞基及NF-κB和MLCK通路來(lái)發(fā)揮作用的。
[Abstract]:Objective to investigate the protective effect of vagal electrical stimulation activated cholinergic anti-inflammatory pathway on tight junction of intestinal epithelial cells and blood gas barrier of lung in endotoxemia mice and its possible mechanism. Methods male Balb/c mice were injected with lipid intraperitoneally. The model of endotoxemia was established by 10 mg / kg polysaccharide. The mice were randomly divided into 4 groups: 1) sham-operated group. The vagus nerve was exposed to isolated vagus nerve but not stimulated by electric stimulation. The rats were given normal saline 0.25 mL intraperitoneal injection of Pao 2) endotoxemia group, exposure to isolated vagus nerve but not electric stimulation, and intraperitoneal injection of lipopolysaccharide 10 mg / kg 3) vagus nerve stimulation group. After intraperitoneal injection of lipopolysaccharide (LPS), 5% pentobarbital sodium was injected intraperitoneally to anesthetize the right vagus nerve. The right vagus nerve was separated from the right vagus nerve, and the right vagus nerve was stimulated by the vagus nerve electrical stimulator for 10 minutes. Subcutaneously, 偽 -BGT 0.5 渭 g / mouse was given 20 min before vagus nerve stimulation. After 12 hours of intraperitoneal injection of lipopolysaccharide, the ileum and lung tissues of mice were collected. Results the levels of FITC-Dextranan in endotoxemia group and 偽 -BGT group were higher than those in sham operation group. The level of FITC-Dextran in endotoxemia group and 偽 -BGT group was higher than that in vagal nerve stimulation group, and the difference was statistically significant (P 0.05). The level of occludin in endotoxemia group was lower than that in sham operation group. The level of occludin in intestinal tissue was lower than that in sham operation group (P 0.05), the level of occludin in 偽 -BGT group was lower than that in sham operation group (P 0.05), the level of occludin in intestinal tissue was lower than that in sham operation group (P 0.05), and the level of vagus nerve was higher in intestinal tissue than that in sham operation group (P 0.05). The level of occludin in lung tissue of electrical stimulation group was higher than that of endotoxemia group and 偽 -BGT group, and the level of NF- 魏 B was lower in electric stimulation group than that in LPS group and 偽 -BGT group. The level of occludin in intestinal tissue was higher than that in endotoxemia group and 偽 -BGT group, and the level of NF- 魏 B in intestinal tissue was lower than that in LPS group and 偽 -BGT group. Conclusion the permeability of blood gas barrier of intestinal epithelium and lung in mice with endotoxemia by vagal nerve stimulation activated cholinergic anti-inflammatory pathway is lower than that in LPS group and 偽 -BGT group. The protection is mediated by nicotinic acetylcholine receptor 偽 7 subunit and NF- 魏 B and MLCK pathways.
【作者單位】: 河南大學(xué)淮河醫(yī)院急診科;河南大學(xué)淮河醫(yī)院神經(jīng)內(nèi)科;河南大學(xué)淮河醫(yī)院呼吸科;
【基金】:河南省教育廳科學(xué)技術(shù)研究重點(diǎn)項(xiàng)目(編號(hào):16A320067)
【分類(lèi)號(hào)】:R459.7


本文編號(hào):1618880


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