安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
ACTA UNIVERSITY MEDICINALIS ANHUI
2015年
4期
458-462
,共5页
李菡%姜宝珍%刘泽玉%陈伟%崔正森%杨青%武前枝%倪琛琛%张志红
李菡%薑寶珍%劉澤玉%陳偉%崔正森%楊青%武前枝%倪琛琛%張誌紅
리함%강보진%류택옥%진위%최정삼%양청%무전지%예침침%장지홍
机械通气%急性肺损伤%高迁移率族蛋白B1%Toll样受体
機械通氣%急性肺損傷%高遷移率族蛋白B1%Toll樣受體
궤계통기%급성폐손상%고천이솔족단백B1%Toll양수체
mechanical ventilation%acute lung injury%high-mobility group box protein 1%Toll-like receptors
目的:探讨高迁移率族蛋白B1(HMGB1)/Toll样受体(TLRs)信号通路在大鼠机械通气肺损伤(VILI)中的作用机制。方法32只健康SD大鼠随机分为4组:正常对照组( N组)不行机械通气,保留自主呼吸;高氧流量组( HN组)氧流量7 L/min;小潮气量机械通气组( LV组)潮气量7 ml/kg;大潮气量机械通气组( HV组)潮气量30 ml/kg。通气4 h后处死动物取肺组织,HE染色观察各组肺组织损伤情况,检测支气管肺泡灌洗液( BALF)中白细胞( WBC)计数、肺湿重干重比值( W/D);ELISA法检测BALF中IL-6、TNF-α、HMGB1水平;Western blot法检测肺组织HMGB1、TLR2、TLR4蛋白的表达。应用单因素方差分析及两样本均数t检验进行不同组间的比较。结果与N组相比,HV组及HN组大鼠肺W/D, BALF中WBC计数,BALF中HMGB1、TNF-α、IL-6水平以及HMGB1、TLR2、TLR4蛋白表达均显著增加,差异有统计学意义(P<0.05);LV组上述各指标与N组相比差异无统计学意义。结论大潮气量机械通气及高氧流量通气均可引起大鼠肺组织急性炎症反应,其机制可能与HMGB1/TLRs信号通路激活有关。
目的:探討高遷移率族蛋白B1(HMGB1)/Toll樣受體(TLRs)信號通路在大鼠機械通氣肺損傷(VILI)中的作用機製。方法32隻健康SD大鼠隨機分為4組:正常對照組( N組)不行機械通氣,保留自主呼吸;高氧流量組( HN組)氧流量7 L/min;小潮氣量機械通氣組( LV組)潮氣量7 ml/kg;大潮氣量機械通氣組( HV組)潮氣量30 ml/kg。通氣4 h後處死動物取肺組織,HE染色觀察各組肺組織損傷情況,檢測支氣管肺泡灌洗液( BALF)中白細胞( WBC)計數、肺濕重榦重比值( W/D);ELISA法檢測BALF中IL-6、TNF-α、HMGB1水平;Western blot法檢測肺組織HMGB1、TLR2、TLR4蛋白的錶達。應用單因素方差分析及兩樣本均數t檢驗進行不同組間的比較。結果與N組相比,HV組及HN組大鼠肺W/D, BALF中WBC計數,BALF中HMGB1、TNF-α、IL-6水平以及HMGB1、TLR2、TLR4蛋白錶達均顯著增加,差異有統計學意義(P<0.05);LV組上述各指標與N組相比差異無統計學意義。結論大潮氣量機械通氣及高氧流量通氣均可引起大鼠肺組織急性炎癥反應,其機製可能與HMGB1/TLRs信號通路激活有關。
목적:탐토고천이솔족단백B1(HMGB1)/Toll양수체(TLRs)신호통로재대서궤계통기폐손상(VILI)중적작용궤제。방법32지건강SD대서수궤분위4조:정상대조조( N조)불행궤계통기,보류자주호흡;고양류량조( HN조)양류량7 L/min;소조기량궤계통기조( LV조)조기량7 ml/kg;대조기량궤계통기조( HV조)조기량30 ml/kg。통기4 h후처사동물취폐조직,HE염색관찰각조폐조직손상정황,검측지기관폐포관세액( BALF)중백세포( WBC)계수、폐습중간중비치( W/D);ELISA법검측BALF중IL-6、TNF-α、HMGB1수평;Western blot법검측폐조직HMGB1、TLR2、TLR4단백적표체。응용단인소방차분석급량양본균수t검험진행불동조간적비교。결과여N조상비,HV조급HN조대서폐W/D, BALF중WBC계수,BALF중HMGB1、TNF-α、IL-6수평이급HMGB1、TLR2、TLR4단백표체균현저증가,차이유통계학의의(P<0.05);LV조상술각지표여N조상비차이무통계학의의。결론대조기량궤계통기급고양류량통기균가인기대서폐조직급성염증반응,기궤제가능여HMGB1/TLRs신호통로격활유관。
Objective The aim of this experiment was to investigate the role of high-mobility group box protein 1 (HMGB1)/Toll-like receptors ( TLRs) signaling pathway in mechanical ventilation lung injury. Methods 32 healthy male SD rats were randomly divided into the following 4 groups according to tidal volume and the concentra-tion of inhaled oxygen:room air inhalation without mechanical ventilation ( N);high concentration of oxygen inhala-tion (50%) without mechanical ventilation ( HN);low tidal volume ventilation with room air inhalation ( LV) (7 ml/kg);high tidal volume ventilation with room air inhalation ( HV) (30 ml/kg) . The ventilation lasted for four hours. Then WBC in BALF and the lung W/D were detected. The adapted ELISA was used to determine the con-centrations of HMGB1, tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6)in BALF from rat. The histologi-cal changes of lung tissue were observed by HE staining. The expressions of HMGB1, TLR4 and TLR2 in lung tis-sue of all rats were detected by western blot. Results HMGB1, TLR2 and TLR4 expressions, the concentrations of HMGB1, TNF-α and IL-6 in BALF, the WBC in BALF and the lung W/D were significantly higher in HV group and HN group (P<0. 05). While they were no significant differences in LV group. Conclusion These findings demonstrated that high tidal volume ventilation and high concentration of oxygen inhalation could aggravate lung in-jury in rats through HMGB1/TLRs signaling pathway.