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CJAP ›› 2018, Vol. 34 ›› Issue (4): 299-303.doi: 10.12047/j.cjap.5651.2018.069

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Effect of particulate matter 2.5 at urban centre of Hangzhou on lung impairment in rats

TIAN Cheng-yuan1, YAN Ming1, ZHANG yun2, LIU Ke-zhou1, GUO Miao1, SUN Yong-hong3, XUE Ling-yun1, ZHU Lei1, XU Ying1   

  1. 1. Department of Biomedical Engineering, College of Life Information Science and Instrument Engineering, Hangzhou Dianzi University, Hangzhou 310018;
    2. Department of Basic Medicine, College of Medicine, Shaoxing University, Shaoxing 312000;
    2. College of Medicine, Shaoxing University, Shaoxing 312000;
    3. Zhejiang Provincial Key Laboratory of Cardio-Cerebral Vascular Detection Technology and Medical Effectiveness Appraisal, Department of Biomedical Engineering, College of Biomedical engineering and Instrument Science, Zhejiang University, Hangzhou 310027, China
  • Received:2017-11-13 Revised:2018-02-08 Online:2018-07-28 Published:2019-02-21
  • Supported by:
    国家自然科学基金(81700936,61871165);国家自然科学基金联合基金项目(U1609218);浙江省自然科学基金(LY15H180012,LY17H060007);浙江省科技厅公益项目(2016C33078)

Abstract: Objective: To explore the effect of ambient particle matter 2.5 (PM2.5) collected in the urban center of Hangzhou on the lung injury of rats and on the activating of endoplasmic reticulum pathway. Methods: PM2.5 samples were collected on quartz fiber filters using a PM2.5 high-volume air sampler in the urban area of Hangzhou. The collected PM2.5 particles were extracted in ultrapure water and concentrated by vacuum freeze-drying. Twenty-four male Sprague-Dawly (SD) rats were randomly divided into 3 groups:saline control group, low dose PM2.5 exposure group (5 mg/kg BW) and high dose PM2.5 exposure groups (25 mg/kg BW). Each group received intratracheal instillation of PM2.5, once a week for 4 weeks. Twenty-four hours after the last exposure, the rats were narcotized and sacrificed, left lung was isolated and fixed with 4% paraformaldehyde for histopathological detection. The bronchoalveolar lavage fluid (BALF) was collected from the right lung. The total antioxidant capacity (T-AOC) level, the activities of superoxide dismutase (SOD) and lactic dehydrogenase (LDH) in BALF were detected by chemical colorimetry. The level of tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β) and interleukin-6 (IL-6) cytokines in BALF was measured by enzyme linked immunosorbent assay (ELISA). And the protein expressions of glucose-regulated protein 78 (GRP78), phosphorylated protein kinase receptor-like endoplasmic reticulum kinase (p-PERK), phosphorylated eukaryotic translation initiation factor (p-eIF2α), transcription factors C/EBP homologue protein (CHOP), inositol-requiring enzyme 1α (IRE1α) and X-box binding protein 1 (XBP1) in lung tissue were determined by Western blotting. Results: Compared with control group, rats in both low dose (5 mg/kg) and high dose (25 mg/kg) PM2.5-treated groups showed obviously dose-dependent pulmonary toxicity including thickening of alveolar walls, narrowing of alveolar space, interstitial hyperplasia and inflammatory cell infiltration. Compared with control group, T-AOC level and the SOD activity in BALF in both PM2.5-treated groups were decreased dose-dependently (P<0.05), whereas the LDH activity in BALF were increased in a dose-dependent manner (P<0.05). Exposure to PM2.5 resulted in a increasing of the release of proinflammatory cytokines including TNF-α, IL-1β and IL-6 in rat lung in a dose-dependent manner (P<0.05). The levels of GRP78, p-PERK, p-eIF2α, CHOP, IRE1α and spliced XBP1 (XBP1-S) were significantly up-regulated, whereas the level of unspliced XBP1 (XBP1-U) was down-regulated in the rat lung tissue of high-dose PM2.5 treated group. Conclusion: The PM2.5 in the urban area of Hangzhou can significantly cause lung inflammatory injury in rats. Both oxidative stress and activation of ER stress pathways may be related to such PM2.5 inhalation-induced lung inflammatory injury.

Key words: ambient particle matter 2.5, rat, lung injury, inflammatory response, oxidative stress, ER stress

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