期刊
INTERNATIONAL IMMUNOPHARMACOLOGY
卷 81, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.intimp.2020.106261
关键词
COPD; STS; Acute exacerbation; Cigarette smoke
资金
- National Key RD Project [2016YFC0903700]
- National Natural Science Foundation of China [81520108001, 81770043, 81560013, 81800072, 81703792, 81900033, 81220108001]
- 973 Key Scheme of China [2015CB553406]
- China Postdoctoral Science Foundation [2017M612637, 2018T110860]
- Guangzhou Science and Technology Programs for Science Study [201607020030, 201804010052]
- Guangdong Province Universities and Colleges Key Grant for Innovative Research [cxzd1142]
- Guangzhou Department of Education [1201620007, 13C08, 12A001S, 1201630095]
- Project of State Key Laboratory of Respiratory Disease [SKLRD-QN-201706, SKLRD-QN-201917, SKLRD-OP-201808]
- Local Innovative and Research Teams Project of Guangdong Pearl River Talents Program [2017BT01S155]
- Major Science and Technology Projects of Inner Mongolia Autonomous Region
- Guangdong Province Universities and Colleges Pearl River Scholar Funded Scheme (2014)
Exacerbation of chronic obstructive pulmonary disease (COPD) is characterized by acute airway inflammation and mucus hypersecretion, which is by far the most costly aspect of its management. Thus, it is essential to develop therapeutics with low side effects for CODP exacerbation. Sodium tanshinone IIA sulfonate (STS) is a water-soluble derivative of tanshinone IIA isolated as the major active component of Chinese herbal medicine Danshen. Although it possesses anti-inflammatory, anti-oxidative and anti-apoptotic properties, it remains unknown whether STS protects against COPD exacerbation. In this study, we challenged cigarette smoke (CS)-exposed mice with lipopolysaccharide (LPS), and then treated these mice with STS. We found that STS significantly ameliorated pulmonary inflammatory responses, mucus hypersecretion and lung function decline in CS-exposed mice challenged with LPS. STS treatment also significantly attenuated increased IL-6 and IL-8 releases from cigarette smoke extract (CSE)-treated human bronchial epithelial cells (16HBE) challenged with LPS. Mechanistically, STS reduced activation of ERK1/2 and NF-kappa B in lungs of CS-exposed mice and CSE-treated 16HBE cells challenged with LPS. Taken together, STS protects against acute exacerbation of CS-induced lung injury, which provides a promising and potential therapeutic avenue to halt acute exacerbation of COPD.
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