Short-interval exposure to ambient fine particulate matter (PM2.5) exacerbates the susceptibility of pulmonary damage in setting of lung ischemia-reperfusion injury in rodent: Pharmacomodulation of melatonin - 04/04/19

Doi : 10.1016/j.biopha.2019.108737

Fan-Yen Lee ^a,^b,^{^{1
These authors have contributed equally and share first authorship.}}, Mel S. Lee ^c,^{^{1
These authors have contributed equally and share first authorship.}}, Christopher Glenn Wallace ^d, Chi-Ruei Huang ^e, Chi-Hsiang Chu ^f, Zhi-Hong Wen ^g, Jhih-Hong Huang ^h,ⁱ, Xue-Sheng Chen ^h,ⁱ, Chia C. Wang ^h,^i,^⁎,^{^{2
These authors have contributed.}} , Hon-Kan Yip ^e,^j,^k,^l,^m,^⁎,^{^{2
These authors have contributed.}}
^a Division of thoracic and Cardiovascular Surgery, Department of Surgery, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, 83301, Taiwan, ROC
^b Division of Cardiovascular Surgery, Department of Surgery, Tri-Service General Hospital, National Defense Medical Center, Taipei, 114, Taiwan, ROC
^c Department of Orthopedics, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, 83301, Taiwan, ROC
^d Department of Plastic Surgery, University Hospital of South Manchester, Manchester, United Kingdom
^e Division of Cardiology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Kaohsiung, 83301, Taiwan, ROC
^f Clinical Trial Center, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, 83301, Taiwan, ROC
^g Department of Marine Biotechnology and Resources, National Sun Yat-sen University, Kaohsiung, 80424, Taiwan, ROC
^h Department of Chemistry, National Sun Yat-sen University, Kaohsiung, Taiwan 804, Taiwan, ROC
ⁱ Aerosol Science Research Center, National Sun Yat-sen University, Kaohsiung, Taiwan 804, Taiwan, ROC
^j Institute for Translational Research in Biomedicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, 83301, Taiwan, ROC
^k Center for Shockwave Medicine and Tissue Engineering, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, 83301, Taiwan, ROC
^l Department of Medical Research, China Medical University Hospital, China Medical University, Taichung, 40402, Taiwan, ROC
^m Department of Nursing, Asia University, Taichung, 41354, Taiwan, ROC

^⁎Corresponding author.

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Abstract

This study tested the hypothesis that exposure to ambient fine particulate matter (PM_2.5) pollution increased susceptibility of rat lung to damage from acute ischemia-reperfusion (IR) injury that was reversed by melatonin (Mel) treatment. Male-adult SD rats (n = 30) were categorized into group 1 (normal control), group 2 (PM_2.5 only), group 3 (IR only at day 8 after PM_2.5 exposure), group 4 (PM_2.5 + IR) and group 5 (PM_2.5 + IR + Mel), and all animals were sacrificed by day 10 after PM_2.5 exposure. Oxygen saturation (%) was significantly higher in group 1 than in other groups and significantly lower in group 4 than in groups 2, 3 and 5 but it did not differ among the latter three groups (p < 0.01). Pulmonary protein expressions of inflammation (MMP-9/TNF-α/NF-kB), oxidative stress (NOX-1/NOX-2/oxidized protein), apoptosis (mitochondrial-Bax/caspase-3/PARP) and fibrosis were lowest in group 1, highest in group 4, significantly higher in group 5 than in groups 2 and 3 (all p < 0.0001), but they did not differ between groups 2 and 3. Inflammatory cell infiltration in lung parenchyma, specific inflammatory cell surface markers (CD14+, F4/88+), allergic inflammatory cells (IgE+, eosinophil+), number of goblet cells, thickness of tracheal epithelial layer and fibrotic area exhibited an identical pattern of protein expressions to inflammation among the five groups (all p < 0.0001). In conclusion, lung parenchymal damage and a rigorous inflammatory response were identified in rodent even with short-term PM_2.5 exposure.

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Keywords : Acute exposure of PM_2.5, Lung parenchymal damage, Inflammation, Oxidative stress

Plan

Introduction

Materials and methods

Ethics

Protocol and protocol of acute lung IR induction (refer to Supplementary Fig. 1)

Equipment and exposure to PM_2.5 (refer to Supplementary Fig. 1)

Animal grouping

Western blot analysis

Immunohistochemical and immunofluorescent studies

Histological study for identification of fibrosis area

Statistical analysis

Results

Arterial oxygen saturation, inflammatory cell infiltration and thickness of tracheal epithelial layer by day 10 after PM_2.5 exposure ()

Eosinophils and IgE + cell infiltrated in lung parenchyma by day10 after PM_2.5 exposure (, )

Inflammatory cell infiltration in lung parenchyma by day 10 after PM_2.5 exposure (, )

Goblet cell expression in tracheal epithelial layer and fibrosis in lung parenchyma by day 10 after PM_2.5 exposure (, )

The protein expressions of inflammation, oxidative stress and anti-oxidants in lung parenchyma by day 10 after PM_2.5 exposure ()

The protein expressions of apoptotic and fibrotic biomarkers in lung parenchyma by day 10 after PM_2.5 exposure ()

Discussion

Study limitations

Conflicts of interest

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Short-interval exposure to ambient fine particulate matter (PM2.5) exacerbates the susceptibility of pulmonary damage in setting of lung ischemia-reperfusion injury in rodent: Pharmacomodulation of melatonin - 04/04/19

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