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Effects of short-term exposure to PM2.5on chronic airway inflammation and oxidative stress of passive smoking rats

HU Jian-rong1,2, XU Hua-jun1, LI Qing-yun1, LI Chun-lei3,SUN Xian-wen1, ZHANG Xiu-juan1   

  1. 1.Department of Respiratory Medicine, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200025, China; 2.Department of Respiratory Medicine, Renji Hospital Jiading Branch, Shanghai Jiao Tong University School of Medicine, Shanghai 201800, China; 3.Department of Environmental Science and Engineering, Fudan University, Shanghai 200433, China
  • Online:2014-05-28 Published:2014-05-30
  • Supported by:

    Innovation Program of Science and Technology Commission of Shanghai Municipality,10231203902; Scientific Research Foundation of Health Bureau of Jiading District of Shanghai, 2013-KY-004

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Abstract:

Objective To explore the effects of short-term exposure to PM2.5 on the chronic airway inflammation and oxidative stress of passive smoking rats and the possible mechanisms. Methods Forty eight male Wistar 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) PM2.5 exposure group (n=12), and high dose (5 mg/ mL) PM2.5 exposure 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-AOC, MDA, GSH-Px, and CAT in 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 PM2.5 exposure group was significantly higher than that of the low dose PM2.5 exposure 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). Compared to the normal control group, the IL-6 and MDA levels of BALF of the passive smoking model group were significantly increased and the T-AOC, GSH-Px, and CAT levels were significantly decreased. The differences were statistically significant (P<0.05). Compared to the simple passive smoking group, the IL-6 and MDA levels of the high dose PM2.5 exposure group were significantly increased and the T-AOC, GSH-Px, and CAT levels 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 PM2.5 exposure group was further exacerbated. The electron microscopy showed that the ultrastructure of type Ⅱ had obvious changes. Conclusion Short-term exposure to PM2.5 can aggravate the chronic airway inflammation and oxidative stress of passive smoking rats.

Key words: PM2.5, chronic airway inflammation, oxidative stress