【摘要】 目的探讨PM2.5短期暴露对被动吸烟大鼠慢性气道炎症和氧化应激反应的影响及可能机制。方法48只雄性Wistar大鼠分为正常对照组(n=12)和被动吸烟模型组(n=36),后者在给予被动吸烟45 d后再随机分为单纯被动吸烟组、低剂量(1.25 mg/mL)PM2.5暴露组和高剂量(5 mg/mL)PM2.5暴露组(n=12)。在末次PM2.5染毒24 h时点,测定大鼠肺功能;收集支气管-肺泡灌洗液(BALF),细胞涂片及吉姆萨(Giemsa)染色后进行细胞计数及分类,对BALF中白介素-6(IL-6)、丙二醛(MDA)、总抗氧化能力(T-AOC)、谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)等指标进行检测;取左肺上叶肺组织,利用光学显微镜(光镜)和透射电子显微镜(透射电镜)观察肺组织学改变和细胞超微结构。结果单纯被动吸烟组和PM2.5暴露组BALF中白细胞总数均显著高于正常对照组(P<0.05),高剂量PM2.5暴露组中性粒细胞百分比显著高于低剂量PM2.5暴露组(P<0.05)。随着PM2.5暴露浓度的升高,大鼠肺功能参数显著降低(P<0.05)。与正常对照组比较,单纯被动吸烟组和PM2.5暴露组BALF中IL-6和MDA水平显著升高,T-AOC、GSH-Px和CAT水平显著降低,差异均有统计学意义(P<0.05);与单纯被动吸烟组比较,高剂量PM2.5暴露组IL-6和MDA水平显著升高,T-AOC、GSH-Px和CAT水平显著降低,差异均有统计学意义(P<0.05)。光镜观察可见单纯被动吸烟组大鼠的支气管壁、血管腔及小气道内中性粒细胞、淋巴细胞、巨噬细胞及嗜酸性粒细胞浸润,肺泡间隔明显变薄或融合,肺泡腔内渗出、充血,肺泡管扩张等结构破坏;PM2.5暴露组上述炎症过程进一步加剧,透射电镜观察发现巨噬细胞和肺泡Ⅱ型上皮细胞超微结构发生明显改变。结论 PM2.5短期暴露可加重被动吸烟大鼠气道慢性炎症及氧化应激反应。更多还原

【Abstract】 Objective To explore the effects of short-term exposure to PM2. 5on the chronic airway inflammation and oxidative stress of passive smoking rats and the possible mechanisms. Methods Forty eight male W istar rats were randomly divided into the normal control group( n = 12) and the passive smoking model group( n = 36). Rats of the latter group were then randomly divided into the simple passive smoking group( n = 12), low dose( 1. 25 mg /mL) PM2. 5exposure group( n = 12), and high dose( 5 mg / mL) PM2. 5exposure group( n = 12) after being given passive smoking for 45 d. The pulmonary function of rats was detected at the time point of 24 h after stopping exposure to PM2. 5. The bronchoalveolar lavage fluid( BALF) was collected and cells were counted and classified after being smeared and stained by Giemsa. IL-6, T-AO C, M DA, GSH-Px,and C ATin BALF were measured. The tissues of left lung lobes were excised and the histological changes and intracellular ultrastructure were observed by the optical microscopy and electron microscopy. Results Total cell count of BALF of the passive smoking model group was significantly higher than that of the normal control group( P < 0. 05). The percentage of neutrophils of high dose PM2. 5exposure group was significantly higher than that of the low dose PM2. 5exposure group( P < 0. 05). The parameters of pulmonary function of rats were significantly decreased with the increase of the exposure concentration of PM2. 5( P < 0. 05). C ompared to the normal control group, the IL-6 and M DA levels of BALF of the passive smoking model group were significantly increased and the T-AO C, GSH-Px, and C ATlevels were significantly decreased. The differences were statistically significant( P < 0. 05). C ompared to the simple passive smoking group, the IL-6 and M DA levels of the high dose PM2. 5exposure group were significantly increased and the T-AO C, GSH-Px, and C ATlevels were significantly decreased. The differences were statistically significant( P < 0. 05). The results of optical microscopy showed that neutrophils, lymphocytes, macrophages, and acidophilic granulocytes in bronchial walls, vessel lumens, and small airways of rats of the passive smoking model group were infiltrated and structural damages were appeared, such as significantly thinned and fused interalveolar septum, effusion and congestion in alveolar spaces, and dilated alveolar ducts. Above inflammatory process of the PM2. 5exposure group was further exacerbated. The electron microscopy showed that the ultrastructure of type Ⅱ had obvious changes. Conclusion Short-term exposure to PM2. 5can aggravate the chronic airway inflammation and oxidative stress of passive smoking rats.更多还原