论文部分内容阅读
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。
Objective To investigate the mechanism of high mobility group box-1 (HMGB1) / Toll-like receptor (TLRs) signaling pathway in rats with mechanical ventilation lung injury (VILI). Methods Thirty-two healthy SD rats were randomly divided into 4 groups: normal control group (N group) did not receive mechanical ventilation and spontaneous breathing, oxygen flow rate was 7 L / min in high oxygen flow group (HN group), low tidal volume mechanical ventilation group Group) tidal volume 7 ml / kg; large tidal volume mechanical ventilation group (HV group) tidal volume 30 ml / kg. Four hours after the ventilation, the animals were sacrificed to take the lung tissue. The lung tissue damage in each group was observed by HE staining. The count of WBC and W / D in bronchoalveolar lavage fluid (BALF) The levels of IL-6, TNF-α and HMGB1 in BALF were detected. The expressions of HMGB1, TLR2 and TLR4 in lung tissue were detected by Western blot. One-way ANOVA and two-sample mean t-test were used to compare the different groups. Results Compared with N group, the WBC counts in W / D and BALF, the levels of HMGB1, TNF-α, IL-6 and the expressions of HMGB1, TLR2 and TLR4 in BALF were significantly increased in HV and HN groups Statistical significance (P <0.05); There was no significant difference between the above indexes in the LV group and the N group. Conclusions Both high tidal volume ventilation and hyperbaric oxygen flow ventilation can cause acute lung inflammation in rats. The mechanism may be related to the activation of HMGB1 / TLRs signaling pathway.