大气污染中气态污染物致大鼠喉黏膜急性损伤的研究

目的 探讨大气污染中气态污染物对大鼠喉黏膜的急性损伤及可能机制。 方法 采用200 g左右健康SPF级SD大鼠12只,随机分为对照组和气态污染物暴露组,每组6只。对照组大鼠饲养于SPF环境中,气态污染物暴露组大鼠呼吸的气体为2016年北京市红色预警期间外界大气经HEPA滤膜过滤颗粒物后的空气,暴露时间为6 d。暴露后处死大鼠,取喉黏膜,检测大鼠喉黏膜的病理学改变及喉黏膜组织细胞因子IL-1β、IL-4、IL-5、IL-6、IL-10、IL-12、IL-13、IL-17a、IFN-γ、TNF-α的表达情况。 结果 与对照组相比,气态污染物暴露组大鼠喉黏膜上皮有不同程度的过度角化、基底细胞排列紊乱;IL-1β、IL-10、IL-13、IL-17a、TNF-α的表达增强(P<0.05);IL-12、IFN-γ的表达减少(P<0.05)。 结论 大气污染中的气态污染物可以引起大鼠喉黏膜损伤,其机制可能与Th1/Th2失衡,呈Th2优势应答有关。

Acute laryngeal mucosa injury in rats induced by gaseous pollutants in the air

Objective To investigate air pollutant-induced acute laryngeal mucosa injury and its possible mechanisms in rats. Methods Twelve healthy SPF Sprague Dawley(SD)rats were randomly and equally divided into control and gas pollutant exposure groups(6 rats in each group). The rats in the control group were fed in an SPF environment, while the rats in the exposure group were exposed to HEPA membrane-filtered air obtained during the red alert period in Beijing in 2016. The rats were sacrificed after exposure to pollutants for 6 days. The pathological changes in rat laryngeal mucosa and IL-1beta, IL-4, IL-5, IL-6, IL-10, IL-12, IL-13, IL-17a, IFN-gamma, and TNF-alpha cytokine expression were then detected. Results The laryngeal mucosa epithelium of rats exposed to air pollutants showed hyperkeratosis and basal cell disorder of varying degrees. IL-1beta, IL-10, IL-13, IL-17a, and TNF-alpha expression also increased (P<0.05) and IL-12 and IFN-gamma expression decreased (P<0.05) in rats exposed to air pollutants when compared to the control group. Conclusion Gas pollutants in the air can cause laryngeal mucosa injury in rats, and its mechanism may be related to Th1/Th2 imbalance, which is a Th2 dominant response.