Haematococcus pluvialis alleviates bleomycin-induced pulmonary fibrosis in mice by inhibiting transformation of lung fibroblasts into myofibroblast.
10.12122/j.issn.1673-4254.2025.08.12
- Author:
Xiao ZHANG
1
;
Jingzhou MAN
1
;
Yong ZHANG
2
;
YunJian ZHENG
2
;
Heping WANG
1
;
Yijun YUAN
1
;
Xi XIE
1
Author Information
1. Key Laboratory of Tropical Biological Resources of Ministry of Education, School of Pharmaceutical Sciences, Hainan University, Haikou 570228, China.
2. Alphy Biotechnology (Jiaxing) Co., LTD, Jiaxing 314422, China.
- Publication Type:Journal Article
- Keywords:
Haematococcus pluvialis;
bleomycin;
fibroblast;
pulmonary fibrosis
- MeSH:
Animals;
Pulmonary Fibrosis/chemically induced*;
Bleomycin/adverse effects*;
Mice, Inbred C57BL;
Male;
Mice;
Fibroblasts/drug effects*;
Lung/pathology*;
Transforming Growth Factor beta1/pharmacology*;
Myofibroblasts/drug effects*;
Humans;
Pyridones
- From:
Journal of Southern Medical University
2025;45(8):1672-1681
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVES:To investigate the effect of Haematococcus pluvialis (HP) on bleomycin (BLM)-induced pulmonary fibrosis in mice and on TGF-β1-induced human fetal lung fibroblasts (HFL1).
METHODS:Thirty male C57BL/6 mice were randomly divided into control group, BLM-induced pulmonary fibrosis model group, low- and high-dose HP treatment groups (3 and 21 mg/kg, respectively), and 300 mg/kg pirfenidone (positive control) group. The effects of drug treatment for 21 days were assessed by examining respiratory function, lung histopathology, and expression of fibrosis markers in the lung tissues of the mouse models. In TGF-β1-induced HFL1 cell cultures, the effects of treatment with 120, 180 and 240 μg/mL HP or 1.85 μg/mL pirfenidone for 48 h on expression levels of fibrosis markers were evaluated. Transcriptome analysis was carried out using the control cells and cells treated with TGF-β1 and 240 μg/mL HP.
RESULTS:HP obviously alleviated BLM-induced lung function damage and fibrotic changes in mice, evidenced by improved respiratory function, lung tissue morphology and structure, inflammatory infiltration, and collagen deposition and reduced expressions of fibrotic proteins. HP at the high dose produced similar effect to PFD. In TGF-β1-induced HFL1 cells, treatment with 240 μg/mL HP significantly reduced the mRNA and protein expression levels of α-SMA and FN. Transcriptome analysis revealed that multiple key genes and pathways mediated the protective effect of HP against pulmonary fibrosis.
CONCLUSIONS:HP alleviates pulmonary fibrosis in both the mouse model and cell model, possibly as the result of the synergistic effects of its multiple active components.
