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An Experimental System to Study Mechanotransduction in Fetal Lung Cells
Published on: February 16, 2012
Fucoidan attenuates hyperoxia-induced lung injury in newborn rats by mediating lung fibroblasts differentiate into
Yan Zhang1, Hengjian Du2, Xuelian Yu1
1Department of Geriatric Medicine, Sichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital, University Hospital of Electronic Science & Technology, Chengdu, China.
Background:
Hyperoxia-induced lung injury is one of the most common and frequent diseases in premature infants and may develop into bronchopulmonary dysplasia (BPD). Fucoidan, extracted from brown seaweed and brown algae, has anti-apoptosis, antioxidative and anti-fibrosis effects. This study aimed to explore whether fucoidan could alleviate hyperoxia-induced lung injury in newborn rats.
Methods:
Lung wet-weight/dry-weight (W/D) ratio, total protein (TP) content, total cell counts, and lactate dehydrogenase (LDH) levels are used to evaluate lung injury. Masson staining is used to evaluate lung fibrotic. Tunnel assay and Hoechst 33258 assay were used to evaluate apoptosis. The levels of serum superoxide dismutase (SOD), malondialdehyde (MDA), and glutathione (GSH) were measured using ELISA to assess oxidative stress. Western blot assay was used to detect apoptosis-related proteins Bcl-1, Bax, and myofibroblast proteins α-SMA.
Results:
The data indicating fucoidan treatment remarkably reduces the lung W/D ratio and TP content, total cell counts, and LDH levels in bronchoalveolar lavage fluid (BALF). Also, fucoidan treatment significantly inhibited cell apoptosis with the elevated expression of Bcl-2/Bax in cultured lung fibroblasts. Moreover, treatment with fucoidan suppressed the levels of MDA significantly and elevated the level of SOD and GSH, showing that oxidative stress was restrained by fucoidan. Furthermore, the decreased expression levels of α-SMA and collagen I was detected in fibroblast treated with fucoidan.
Conclusions:
These data suggest fucoidan may protect the lung from hyperoxia via suppressing cell apoptosis, mitigating oxidative stress, and inhibiting lung fibroblasts from differentiating into myofibroblasts.
