Pine bark extract (Pycnogenol®) suppresses cigarette smoke-induced fibrotic response via transforming growth factor-β1/Smad family member 2/3 signaling

Laboratory Animal Research

Young-Kwon Cho¹  In-Sik Shin²  Dong-Ho Shin²  Je-Won Ko²  Jong-Choon Kim²  Na-Rae Shin²  Sung-Hyeuk Park²  Joong-Sun Kim³ 

[1] College of Health Sciences, Cheongju University;College of Veterinary Medicine (BK21 Plus Project Team), Chonnam National University;Research Center, Dongnam Institute of Radiological and Medical Sciences (DIRAMS);

关键词: Pycnogenol;    chronic obstructive pulmonary disease;    cigarette smoke;    collagen deposition;    transforming growth factor-β1/Smad family member 2/3;   

DOI  :  10.5625/lar.2017.33.2.76

来源: DOAJ

【 摘 要 】

Abstract Chronic obstructive pulmonary diseases (COPD) is an important disease featured as intense inflammation, protease imbalance, and air flow limitation and mainly induced by cigarette smoke (CS). In present study, we explored the effects of Pycnogenol® (PYC, pine bark extract) on pulmonary fibrosis caused by CS+lipopolysaccharide (LPS) exposure. Mice were treated with LPS intranasally on day 12 and 26, followed by CS exposure for 1 h/day (8 cigarettes per day) for 4 weeks. One hour before CS exposure, 10 and 20 mg/kg of PYC were administered by oral gavage for 4 weeks. PYC effectively reduced the number of inflammatory cells and proinflammatory mediators caused by CS+LPS exposure in bronchoalveolar lavage fluid. PYC inhibited the collagen deposition on lung tissue caused by CS+LPS exposure, as evidenced by Masson’s trichrome stain. Furthermore, transforming growth factor-β1 (TGF-β1) expression and Smad family member 2/3 (Smad 2/3) phosphorylation were effectively suppressed by PYC treatment. PYC markedly reduced the collagen deposition caused by CS+LPS exposure, which was closely involved in TGF-β1/Smad 2/3 signaling, which is associated with pulmonary fibrotic change. These findings suggest that treatment with PYC could be a therapeutic strategy for controlling COPD progression.

【 授权许可】

Unknown