白及对PM2.5致大鼠肺损伤的治疗作用

Therapeutic effect of Bletilla striata on lung injury induced by PM2.5 in rats

目的:研究白及对PM2.5致大鼠肺损伤的治疗作用。方法:40只雄性Wistar大鼠随机分为正常组、模型组和白及低、中、高剂量组,每组8只。除正常组外,其余大鼠鼻腔滴注PM2.5混悬液造模。8周后各组予相应药物灌胃。4周后检测大鼠肺泡灌洗液(BALF)中TNF-α、IL-6及活性氧(ROS)的表达;外周血游离DNA及髓过氧化物酶(MPO)-DNA复合物的表达;免疫荧光染色法检测肺组织中性粒细胞胞外诱捕网(NETs)的生成;光镜下观察肺组织结构。结果:与正常组比较,模型组大鼠BALF中TNF-α、IL-6和ROS显著升高(P<0.01),血浆游离DNA及MPO-DNA显著增加(P<0.01),肺组织NETs大量生成,病理损伤明显;与模型组比较,白及各剂量组大鼠BALF中TNF-α、IL-6和ROS显著降低(P<0.05,P<0.01),血浆游离DNA及MPO-DNA显著减少(P<0.05,P<0.01),肺组织NETs生成减少,病理损伤减轻。结论:白及能通过抗炎抗氧化作用减少ROS产生,抑制NETs生成,发挥对PM2.5诱导的大鼠肺损伤的治疗作用。

Objective: To investigate the therapeutic effect of Bletilla striata on PM2.5-induced lung injury in rats. Methods: Forty rats were randomly divided into the normal group, model group, and three different dose of Bletilla striata suspension groups, 8 rats in each group. Except for the normal group, the rest rats were injectd with PM2.5 suspension for 8 weeks to established the model of lung injury, then corresponding drugs were administrated. After 4 weeks, the level of TNF-α, IL-6 and reactive oxygen species(ROS) in bronchoalveolar lavage fluid(BALF) and the expressions of free DNA and MPODNA complex in plasma were detected. The expression of neutrophil extracellular traps(NETs) in lung tissue was detected by Immunofluorescence staining, the lung tissue structure was observed under microscope. Results: Compared with the normal group, the levels of TNF-α, IL-6 and ROS in the model group were significantly increased(P<0.01), the amount of free DNA, MPODNA and NETs were significantly increased(P<0.01), pathological damage of lung tissue was obvious. Compared with the model group, the levels of TNF-α, IL-6 and ROS in Bletilla striata administration groups decreased(P<0.05, P<0.01), the contents of free DNA and MPO-DNA were significantly decreased(P<0.05, P<0.01), the generation of NETs in lung tissue was reduced and the pathological damage was alleviated. Conclusion: Bletilla striata can reduce the formation of ROS through anti-inflammatory and anti-oxidative effects, thereby inhibiting the formation of NETs and thus playing the therapeutic role in PM2.5-induced lung injury in rats.