电刺激迷走神经对脂多糖诱导ALI大鼠的肺保护作用

发布时间：2018-03-21 19:26

本文选题：脂多糖　切入点：急性肺损伤　出处：《南昌大学》2017年硕士论文　论文类型：学位论文

【摘要】：目的:检测电刺激迷走神经(VNS)对脂多糖(LPS)诱导的肺损伤大鼠的肺保护作用。方法:健康、清洁的成年雄性SD大鼠(250±20g)60只,由南京鹏晟生物发展有限公司提供,随机分为4组:生理盐水组(NS组)、脂多糖组(LPS组)、迷走神经电刺激组(LPS+VNS组)和迷走神经离断组(LPS+VNB组),每组15只。NS组:在尾静脉注射10ml/kg生理盐水,切开双侧颈动脉鞘,分离双侧迷走神经;LPS组:在尾静脉注射10mg/kg 1%LPS,切开双侧颈动脉鞘,分离双侧迷走神经;LPS+VNS组:在尾静脉注射10mg/kg 1%LPS,切开双侧颈动脉鞘,分离双侧迷走神经,在左侧迷走神经远端连接刺激电极,给予持续电刺激(1mA,1ms和10Hz);LPS+VNB组:在尾静脉注射10mg/kg 1%LPS,切开双侧颈动脉鞘,分离迷走神经,切断双侧迷走神经,在近心端的左侧迷走神经远端连接刺激电极,给予持续电刺激(1mA,1ms和10Hz)。通气120min末,开胸取肺组织,HE染色后在倒置显微镜下观察肺组织病理学变化,western blot检测IL-1、IL-6、IL-10、TNF-α蛋白的表达水平变化;取肺泡灌洗液(BALF)进行流式分析细胞凋亡情况。结果:1、在LPS组中,与NS组比较,BALF中早期和晚期的细胞凋亡率显著增加(P0.05);肺组织中的IL-1、IL-6、IL-10、TNF-α蛋白表达显著上调(P0.05);2、在LPS+VNS组中,与LPS组比较,BALF中早期和晚期的细胞凋亡率明显下降(P0.05),肺组织中的IL-1、IL-6、IL-10、TNF-α蛋白表达显著下调(P0.05);3、在LPS+VNB组中,与LPS组比较,BALF中早期的细胞凋亡率明显下降(P0.05),晚期的细胞凋亡率下降不显著(P0.05),差异无统计学意义,肺组织中的IL-1、IL-10蛋白表达显著下调(P0.05),IL-6蛋白表达量增加(P0.05),TNF-α蛋白表达量下降不显著(P0.05),差异无统计学意义;与LPS+VNS组比较,BALF中早期和晚期的细胞凋亡率明显增加(P0.05),肺组织中的IL-1、IL-6、IL-10、TNF-α蛋白表达显著上调(P0.05)。结论:1、脂多糖可致大鼠肺损伤。2、在脂多糖致肺损伤的大鼠模型中,电刺激迷走神经可逆转肺损伤中的炎症反应,从而发挥肺保护作用,其机制有待进一步研究。
[Abstract]:Objective: to investigate the protective effect of electric stimulation of vagus nerve (VNS) on lung injury induced by lipopolysaccharide (LPS) in rats. Methods: healthy, clean adult male SD rats (250 卤20g)60) were provided by Nanjing Pengsheng Biological Development Co., Ltd. They were randomly divided into 4 groups: normal saline group (NS group), lipopolysaccharide group (LPS group), vagal nerve stimulation group (VNS group) and vagal nerve disconnection group (VNB group). 15 rats in each group were injected 10ml/kg normal saline into tail vein, and bilateral carotid sheath was cut open. In the group of separating bilateral vagus nerve lipopolysaccharide (LPs): injection of 10mg/kg 1 into caudal vein, incision of bilateral carotid sheath, separation of bilateral vagus nerve lipopolysaccharide: injection of 10mg/kg 1 into caudal vein, incision of bilateral carotid sheath, separation of bilateral vagus nerve, At the distal end of the left vagus nerve, the stimulation electrode was connected to the distal part of the vagus nerve, and the continuous electrical stimulation was given for 1 Ms and 10 Hz VNB group. The caudal vein was injected with 10mg/kg 1 LPS1, the bilateral carotid artery sheath was cut open, the vagus nerve was separated, and the bilateral vagus nerve was cut off. At the proximal end of the left vagus nerve, the distal junction of the left vagus nerve was stimulated with continuous electrical stimulation of 1 Ms and 10 Hz. The lung tissues were removed for HE staining at the end of 120min. The histopathological changes of lung tissue were observed under inverted microscope. The expression level of IL-1mA1mA1TNF- 伪 was detected by western blot. Results: in the LPS group, the apoptosis rate in the early and late stages of BALF was significantly higher than that in the NS group, while the expression of IL-6 IL-6, IL-10, TNF- 伪 protein in the lung tissue was significantly up-regulated in the LPS VNS group, while the expression of IL-6 IL-10 TNF- 伪 protein in the lung tissue was significantly up-regulated in the LPS VNS group, while in the LPS VNS group, the apoptosis rate in the early and late stages of BALF was significantly higher than that in the NS group. Compared with the LPS group, the apoptosis rate in the early and late stages of LPS decreased significantly (P 0.05), and the expression of IL-1, IL-6, IL-10, TNF- 伪 in the lung tissue decreased significantly. In the LPS VNB group, the expression of IL-10 TNF- 伪 was significantly down-regulated. Compared with LPS group, the rate of apoptosis in the early stage of LPS was significantly lower than that in the late stage (P 0.05), and there was no significant difference between the two groups. The expression of IL-1T IL-10 in lung tissue decreased significantly (P 0.05) and increased the expression of TNF- 伪. There was no significant difference in the expression of TNF- 伪 (P 0.05). Compared with LPS VNS group, the rate of apoptosis in the early and late stages of LPS VNS was significantly increased, and the expression of IL-1, IL-6, IL-10, TNF- 伪 protein in lung tissue was significantly up-regulated. Conclusion: 1: 1, lipopolysaccharide can induce lung injury in rats, and in the rat model of lung injury induced by lipopolysaccharide. Electrical stimulation of vagus nerve can reverse the inflammatory response in lung injury and thus play a protective role in lung, and its mechanism needs further study.
【学位授予单位】：南昌大学
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R563.8

【参考文献】