Isolation, Characterization, and Anti-Idiopathic Pulmonary Fibrosis Activity of a Fucoidan from <i>Costaria costata</i>
Sijie Wei,
Lihua Geng,
Haoyu Yu,
Jing Wang,
Yang Yue,
Quanbin Zhang,
Ning Wu
Affiliations
Sijie Wei
CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China
Lihua Geng
CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China
Haoyu Yu
CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China
Jing Wang
CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China
Yang Yue
CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China
Quanbin Zhang
CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China
Ning Wu
CAS and Shandong Province Key Laboratory of Experimental Marine Biology, Center for Ocean Mega-Science, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China
Pulmonary fibrosis is a chronic, progressive, and fatal disease of the interstitial lung. There is currently a lack of efficient therapy to reverse the prognosis of patients. In this study, a fucoidan from Costaria costata was isolated, and its anti-idiopathic fibrosis activity was investigated both in vitro and in vivo. The chemical composition analysis showed that C. costata polysaccharide (CCP) consists of galactose and fucose as the main monosaccharides with a sulfate group content of 18.54%. Further study found that CCP could resist TGF-β1-induced epithelial-mesenchymal transition (EMT) in A549 cells by inhibiting the TGF-β/Smad and PI3K/AKT/mTOR signaling pathways. Moreover, in vivo study found that CCP treatment alleviated bleomycin (BLM)-stimulated fibrosis and inflammation in mice lung tissue. In conclusion, the present study suggests that CCP could protect the lung from fibrosis by relieving the EMT process and inflammation in lung cells.
