Low Molecular Weight Fucoidan Inhibits Pulmonary Fibrosis In Vivo and In Vitro via Antioxidant Activity

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Abstract

In this study, sulfated polysaccharides extracted from Laminaria japonica were degraded by free radicals to obtain low molecular weight fucoidan (LMWF). The in vivo and in vitro effects of LMWF on bleomycin-treated pulmonary fibrosis mice and TGF-treated A549 cells, respectively, were evaluated, and the role of antioxidant activity was assessed. H&E, Masson's trichrome, and Sirius red staining results showed that bleomycin induced obvious pathological changes and collagen deposition in the lung tissue of mice. However, LMWF effectively inhibited collagen deposition, and based on immunohistochemistry analyses, LMWF can also inhibit the expression of fibrosis markers. At the same time, LMWF could regulate related antioxidant factors in the lung tissue of pulmonary fibrosis mice and reduce the pressure of oxidative stress. Moreover, LMWF could improve the morphology of cells induced with TGF, which confirmed that LMWF could inhibit fibrosis via antioxidant activity modulation.

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A phase 3 trial of pirfenidone in patients with idiopathic pulmonary fibrosis.

Talmadge E King, Williamson Bradford, Socorro Castro-Bernardini … (2014)

In two of three phase 3 trials, pirfenidone, an oral antifibrotic therapy, reduced disease progression, as measured by the decline in forced vital capacity (FVC) or vital capacity, in patients with idiopathic pulmonary fibrosis; in the third trial, this end point was not achieved. We sought to confirm the beneficial effect of pirfenidone on disease progression in such patients. In this phase 3 study, we randomly assigned 555 patients with idiopathic pulmonary fibrosis to receive either oral pirfenidone (2403 mg per day) or placebo for 52 weeks. The primary end point was the change in FVC or death at week 52. Secondary end points were the 6-minute walk distance, progression-free survival, dyspnea, and death from any cause or from idiopathic pulmonary fibrosis. In the pirfenidone group, as compared with the placebo group, there was a relative reduction of 47.9% in the proportion of patients who had an absolute decline of 10 percentage points or more in the percentage of the predicted FVC or who died; there was also a relative increase of 132.5% in the proportion of patients with no decline in FVC (P<0.001). Pirfenidone reduced the decline in the 6-minute walk distance (P=0.04) and improved progression-free survival (P<0.001). There was no significant between-group difference in dyspnea scores (P=0.16) or in rates of death from any cause (P=0.10) or from idiopathic pulmonary fibrosis (P=0.23). However, in a prespecified pooled analysis incorporating results from two previous phase 3 trials, the between-group difference favoring pirfenidone was significant for death from any cause (P=0.01) and from idiopathic pulmonary fibrosis (P=0.006). Gastrointestinal and skin-related adverse events were more common in the pirfenidone group than in the placebo group but rarely led to treatment discontinuation. Pirfenidone, as compared with placebo, reduced disease progression, as reflected by lung function, exercise tolerance, and progression-free survival, in patients with idiopathic pulmonary fibrosis. Treatment was associated with an acceptable side-effect profile and fewer deaths. (Funded by InterMune; ASCEND ClinicalTrials.gov number, NCT01366209.).

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Nintedanib in Progressive Fibrosing Interstitial Lung Diseases

Kevin R. Flaherty, Athol Wells, Vincent Cottin … (2019)

Preclinical data have suggested that nintedanib, an intracellular inhibitor of tyrosine kinases, inhibits processes involved in the progression of lung fibrosis. Although the efficacy of nintedanib has been shown in idiopathic pulmonary fibrosis, its efficacy across a broad range of fibrosing lung diseases is unknown.

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Idiopathic pulmonary fibrosis.

Luca Richeldi, Harold Collard, Mark G. Jones (2017)

Idiopathic pulmonary fibrosis is a prototype of chronic, progressive, and fibrotic lung disease. Healthy tissue is replaced by altered extracellular matrix and alveolar architecture is destroyed, which leads to decreased lung compliance, disrupted gas exchange, and ultimately respiratory failure and death. In less than a decade, understanding of the pathogenesis and management of this disease has been transformed, and two disease-modifying therapies have been approved, worldwide. In this Seminar, we summarise the presentation, pathophysiology, diagnosis, and treatment options available for patients with idiopathic pulmonary fibrosis. This disease has improved understanding of the mechanisms of lung fibrosis, and offers hope that similar approaches will transform the management of patients with other progressive fibrotic lung diseases.

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Author and article information

Contributors

Xinpeng Li:

ORCID: https://orcid.org/0000-0003-1165-4723

Journal

Journal ID (nlm-ta): Oxid Med Cell Longev

Journal ID (iso-abbrev): Oxid Med Cell Longev

Journal ID (publisher-id): OMCL

Title: Oxidative Medicine and Cellular Longevity

Publisher: Hindawi

ISSN (Print): 1942-0900

ISSN (Electronic): 1942-0994

Publication date Collection: 2022

Publication date (Electronic): 2 March 2022

Volume: 2022

Electronic Location Identifier: 7038834

Affiliations

¹College of Pharmacy, Linyi University, Linyi, Shandong, China

²Chinese Academy of Traditional Chinese Medicine, China

Author notes

Academic Editor: Ryoji Nagai

Author information

Xinpeng Li https://orcid.org/0000-0003-1165-4723

Article

DOI: 10.1155/2022/7038834

PMC ID: 8906950

PubMed ID: 35281460

SO-VID: d16c1ebe-e2c9-48de-bcd4-bdb2a600d3db

License:

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

History

Date received : 5 September 2021

Date revision received : 13 December 2021

Date accepted : 14 February 2022

Funding

Funded by: Innovation and Entrepreneurship Training Program for College Students in Shandong Province

Award ID: S202110452122

Funded by: Key Project at Central Government Level: The Ability Establishment of Sustainable Use for Valuable Chinese Medicine Resources

Low Molecular Weight Fucoidan Inhibits Pulmonary Fibrosis In Vivo and In Vitro via Antioxidant Activity

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Most cited references 40

A phase 3 trial of pirfenidone in patients with idiopathic pulmonary fibrosis.

Nintedanib in Progressive Fibrosing Interstitial Lung Diseases

Idiopathic pulmonary fibrosis.

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