TLR-1，TLR-2在大鼠呼吸机相关性肺损伤肺组织中的表达及其作用的实验研究
发布时间：2019-04-11 08:20
【摘要】：目的探讨在呼吸机相关性肺损伤的大鼠模型中肺组织TLR-1、TLR-2表达的情况。 方法120只SPrague Dawley大鼠随机分成对照组(A组,自主呼吸组)、正常通气组(B组,VT=10ml/kg)、过度通气潮气量组(C组,VT=20ml/kg)及过度通气大潮气量组(D组,VT=40ml/kg),每组30只。各组按通气时间(60min、120min和240min)再随机分为3亚组,每亚组10只。所有大鼠均采用经口气管插管,实验组(B、C、D组)应用小型动物呼吸机予双肺机械通气,对照组(A组)在插管后保持自主呼吸。各组实验结束后,颈总动脉放血处死大鼠,并取肺组织。光镜下观察肺组织的病理改变,利用RT-PCR检测各组肺组织TLR-1mRNA、TLR-2mRNA表达和ELISA检测各组肺组织中TLR-1、TLR-2的浓度。 结果①大鼠肺组织病理学变化：正常通气组和对照组未见明显肺损伤表现；C组在光镜下可见少量肺间质水肿和炎症细胞浸润；D组可见肺组织点状或者片状出血,肺间隔增宽,肺间质明显水肿,肺泡腔融合,大量炎性细胞积聚,部分肺组织有实变；②TLR-1、TLR-2及肺组织TLR-1mRNA、TLR-2mRNA的表达：B、C、D组与A组比较,TLR-1及TLR-1mRNA的表达差异无统计学意义(P0.05),B组与A组比较,TLR-2及TLR-2mRNA的表达差异性无统计学意义(P0.05),C、D组分别与A组比较,TLR-2的表达明显高于对照组,差异有统计学意义(P0.05),D组亚组比较,通气240min明显高于通气60min亚组,差异有统计学意义(P0.05)。 结论大潮气量的机械通气和长时间机械通气会导致VILI,同时,可上调肺组织中TLR-2mRNA表达。
[Abstract]:Objective to investigate the expression of TLR-1,TLR-2 in lung tissue of ventilator-associated lung injury rats. Methods 120 SPrague Dawley rats were randomly divided into three groups: control group (group A, spontaneous breathing group), normal ventilation group (group B, VT=10ml/kg), hyperventilation tidal volume group (group C, VT=20ml/kg) and hyperventilation high tidal volume group (group D, VT=40ml/kg). There are 30 in each group. All groups were randomly divided into 3 subgroups according to ventilation time (60 min, 120 min and 240min), 10 rats in each subgroup. All rats were treated with tracheal intubation. The experimental group (B, C, D) was ventilated with small animal ventilator. The control group (group A) kept breathing autonomously after intubation. At the end of the experiment, the rats were killed by common carotid artery bleeding and lung tissue was obtained. The pathological changes of lung tissue were observed under light microscope. The expression of TLR-1mRNA,TLR-2mRNA in lung tissue was detected by RT-PCR and the concentration of TLR-1,TLR-2 in lung tissue was measured by ELISA. Results (1) pathological changes of rat lung: there was no obvious lung injury in normal ventilation group and control group, and a small amount of pulmonary interstitial edema and inflammatory cell infiltration were observed in group C under light microscope. In group D, punctate or lamellar hemorrhage, widening of pulmonary septum, obvious edema of pulmonary interstitial, fusion of alveolar cavity, accumulation of a large number of inflammatory cells and consolidation of some lung tissues were observed. 2the expression of TLR1, TLR2 and TLR-1mRNA,TLR-2mRNA in lung tissue: there was no significant difference in the expression of TLR-1 and TLR-1mRNA between group B, C, D and A (P0.05 compared with group A, P 0.05). There was no significant difference in the expression of TLR-2 and TLR-2mRNA (P0.05). Compared with group A, the expression of TLR-2 in group C, D was significantly higher than that in group A (P0.05). There was significant difference in expression of TLR-2 (P0.05) between group), D and group A (P0.05). Ventilation 240min was significantly higher than ventilation 60min subgroup, the difference was statistically significant (P0.05). Conclusion large tidal volume mechanical ventilation and long-term mechanical ventilation can lead to VILI, and up-regulate the expression of TLR-2mRNA in lung tissue.
【学位授予单位】：广西医科大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R563
本文编号：2456249
[Abstract]:Objective to investigate the expression of TLR-1,TLR-2 in lung tissue of ventilator-associated lung injury rats. Methods 120 SPrague Dawley rats were randomly divided into three groups: control group (group A, spontaneous breathing group), normal ventilation group (group B, VT=10ml/kg), hyperventilation tidal volume group (group C, VT=20ml/kg) and hyperventilation high tidal volume group (group D, VT=40ml/kg). There are 30 in each group. All groups were randomly divided into 3 subgroups according to ventilation time (60 min, 120 min and 240min), 10 rats in each subgroup. All rats were treated with tracheal intubation. The experimental group (B, C, D) was ventilated with small animal ventilator. The control group (group A) kept breathing autonomously after intubation. At the end of the experiment, the rats were killed by common carotid artery bleeding and lung tissue was obtained. The pathological changes of lung tissue were observed under light microscope. The expression of TLR-1mRNA,TLR-2mRNA in lung tissue was detected by RT-PCR and the concentration of TLR-1,TLR-2 in lung tissue was measured by ELISA. Results (1) pathological changes of rat lung: there was no obvious lung injury in normal ventilation group and control group, and a small amount of pulmonary interstitial edema and inflammatory cell infiltration were observed in group C under light microscope. In group D, punctate or lamellar hemorrhage, widening of pulmonary septum, obvious edema of pulmonary interstitial, fusion of alveolar cavity, accumulation of a large number of inflammatory cells and consolidation of some lung tissues were observed. 2the expression of TLR1, TLR2 and TLR-1mRNA,TLR-2mRNA in lung tissue: there was no significant difference in the expression of TLR-1 and TLR-1mRNA between group B, C, D and A (P0.05 compared with group A, P 0.05). There was no significant difference in the expression of TLR-2 and TLR-2mRNA (P0.05). Compared with group A, the expression of TLR-2 in group C, D was significantly higher than that in group A (P0.05). There was significant difference in expression of TLR-2 (P0.05) between group), D and group A (P0.05). Ventilation 240min was significantly higher than ventilation 60min subgroup, the difference was statistically significant (P0.05). Conclusion large tidal volume mechanical ventilation and long-term mechanical ventilation can lead to VILI, and up-regulate the expression of TLR-2mRNA in lung tissue.
【学位授予单位】：广西医科大学
【学位级别】：硕士
【学位授予年份】：2013
【分类号】：R563
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