大气细颗粒物对大鼠白细胞介素17表达的影响及连花清瘟的干预作用

目的  探讨大气细颗粒物（PM2.5）急性暴露对大鼠肺部损伤的作用，及高、中、低剂量连花清瘟对其的保护作用。方法  48只Wistar大鼠，随机分为4个实验组（PM2.5染尘组及高、中、低剂量连花清瘟干预组）和2个对照组（空白对照组及生理盐水对照组）。由石家庄市环境监测中心提供空气细颗粒物，制备PM2.5悬液，采用气管内滴注法。空白对照组无任何干预措施；生理盐水对照组给予气管滴注生理盐水（1 ml/kg）；染尘组给予一次性气管内滴入PM2.5悬液（7.5 mg/kg）；3组干预组首先分别连续灌胃给予低（生药2 g/kg）、中（生药4 g/kg）、高（生药8 g/kg）剂量的连花清瘟溶液4 d，第4天灌胃给药后分别经气管滴入PM2.5悬液（7.5 mg/kg)。应用酶联免疫分析（ELISA）法测定各实验组动物血清白细胞介素17（IL-17)及肺表面活性蛋白A（SP-A）水平，并在光镜下观察肺组织病理形态变化。结果  空白对照组和生理盐水对照组间血清IL-17及SP-A差异无统计学意义（P >0.05），染尘组血清IL-17及SP-A水平较生理盐水对照组及空白对照组显著升高，差异有统计学意义（P <0.05）；高、中、低剂量干预组较染尘组血清IL-17及SP-A水平均有不同程度降低，中高剂量组差异有统计学意义（P <0.05）。结论  PM2.5急性暴露可以导致大鼠肺部损伤，连花清瘟对肺部损伤有保护作用。

Effect of surrounding fine particulate matter (PM2.5) on IL-17 expression in rats and antagonistic effects of Lianhuaqingwen

Objectives To explore the lung injury of rats due to acute exposure to PM2.5, and to discuss the antagonistic role of Lianhuaqingwen to the injury. Methods Forty-eight healthy adult Wistar rats were randomly assigned into four experimental groups (PM2.5 group, low-dose Lianhuaqingwen group, medium-dose Lianhuaqingwen group and high-dose Lianhuaqingwen group) and two control groups (control group and saline control group). The PM2.5 suspension was prepared with fine particulates provided by Shijiazhuang Environmental Monitoring Center. The rat models were developed by exposure to PM2.5 through intratracheal drip. The saline control group was instilled with saline (1 ml /kg) once; the PM2.5 group was instilled with suspension of PM2.5 via trachea (7.5 mg/kg); the three intervention groups were given diet supplemented with different doses of Lianhuaqingwen (2 g/kg, 4 g/kg and 8 g/kg respectively) for 4 days before drip with suspension of PM2.5. Interleukin 17 (IL-17) and surfactant protein A (SP-A) in the serum were measured using ELASA. Pathological changes of the lungs were observed at the same time. Results The serum levels of IL-17 and SP-A were not significantly different between the saline control group and the control group (P > 0.05). The levels of IL-17 and SP-A in the PM2.5 group were markedly higher than those in the saline control group and the control group (P < 0.05).  The level of IL-17 was significant different between the high-dose Lianhuaqingwen group and the PM2.5 group (P < 0.05), and the level of IL-17 in each intervention group was markedly changed compared with that in the PM2.5 group (P < 0.05). Conclusions The acute exposure to PM2.5 can induce injury to rat''s lungs. Lianhuaqingwen could produce antagonistic effects to inflammatory injury to rat''s lung tissues.