IL-10 ameliorates PM2.5-induced lung injury by activating the AMPK/SIRT1/PGC-1α pathway |
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| Institution: | 1. Department of Respiratory Medicine, The Third Hospital of Hebei Medical University, Shijiazhuang, 050051, Hebei, China;2. Department of Gerontology, Hebei General Hospital, Shijiazhuang, 050051, Hebei, China;3. Department of Urinary Surgery, The First Hospital of Shijiazhuang, Shijiazhuang, 050051, Hebei, China;1. Faculty of Public Health, Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, PR China;2. The Ninth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, PR China;1. Department of Health Toxicology, Xiangya School of Public Health, Central South University, Changsha, Hunan, 410078, China;2. Institute of Environment and Health, Shenzhen Center for Disease Control and Prevention, Shenzhen, Guangdong, 518055, China;3. School of Public Health, University of South China, Hengyang, Hunan, 421001, China;1. Department of Respiratory Medicine, Hospital of Chengdu University of Traditional Chinese Medicine, No. 39 Shi-er-qiao Road, Chengdu 610072, Sichuan Province, People’s Republic of China;2. Department of Geriatrics, Hospital of Chengdu University of Traditional Chinese Medicine, No. 39 Shi-er-qiao Road, Chengdu 610072, Sichuan Province, People’s Republic of China;1. Department of Toxicology and Sanitary Chemistry, School of Public Health, Capital Medical University, Beijing, 100069, PR China;2. Beijing Key Laboratory of Environmental Toxicology, Capital Medical University, Beijing, 100069, PR China;1. Institute of Environmental Science, College of Environmental & Resource Sciences, Shanxi University, Taiyuan, China;2. State Key Laboratory of Environmental and Biological Analysis, Department of Chemistry, Hong Kong Baptist University, Hong Kong SAR, China |
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| Abstract: | Exposure to fine particulate matter with a diameter ≤2.5 μm (PM2.5) can cause a number of respiratory diseases. However, there is currently no safe treatment for PM2.5-induced lung damage. This study investigated the protective effect of IL-10 against lung injury and the possible involvement of AMPK/SIRT1/PGC-1α signaling. The mean diameter, particle size distribution, and zeta potential of PM2.5 samples were assessed using a Zetasizer Nano ZS90 analyzer. Thereafter, Wistar rats were exposed to PM2.5 (1.8, 5.4, or 16.2 mg/kg) alone or high-dose PM2.5 with recombinant rat IL-10 (rrIL-10; 5 μg/rat). Treatment with rrIL-10 ameliorated PM2.5-induced acute lung injury, reduced mitochondrial damage, and inhibited inflammation, oxidative stress, and apoptosis in the PM2.5-treated rats. Moreover, the mRNA and protein expression of AMPK, SIRT1, and PGC-1α were upregulated by rrIL-10 treatment. In conclusion, rrIL-10 protected lung tissues against PM2.5-induced inflammation by reducing oxidative stress and apoptosis via activating AMPK/SIRT1/PGC-1α signaling. |
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| Keywords: | Fine particulate matter AMPK SIRT1 PGC-1α interleukin-10 Lung injury |
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