Astaxanthin inhibits lung fibrosis via down-regulation of TGF-β1-mediated Smads/ERK signaling pathway
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Astaxanthin inhibits lung fibrosis via down-regulation of TGF-β1-mediated Smads/ERK signaling pathway
Journal of Army Medical UniversityVol. 39, Issue 5, Pages: 442-447(2017)
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CLC:R563.13;R595.4;R979.9
Published:2017
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王芳芹,刘涛,张攀,阳群芳,陈晓红.虾青素通过TGF-β1介导的Smads/ERK通路抑制肺纤维化[J].陆军军医大学学报(原第三军医大学学报),2017,39(05 ):442-447. Wang Fangqin,Liu Tao,Zhang Pan,Yang Qunfang,Chen Xiaohong.Astaxanthin inhibits lung fibrosis via down-regulation of TGF-β1-mediated Smads/ERK signaling pathway[J].J Amry Med Univ (J Third Mil Med Univ),2017,39(05 ):442-447.
王芳芹, 刘涛, 张攀, et al. Astaxanthin inhibits lung fibrosis via down-regulation of TGF-β1-mediated Smads/ERK signaling pathway[J]. Journal of Army Medical University, 2017, 39(5): 442-447.
王芳芹,刘涛,张攀,阳群芳,陈晓红.虾青素通过TGF-β1介导的Smads/ERK通路抑制肺纤维化[J].陆军军医大学学报(原第三军医大学学报),2017,39(05 ):442-447. Wang Fangqin,Liu Tao,Zhang Pan,Yang Qunfang,Chen Xiaohong.Astaxanthin inhibits lung fibrosis via down-regulation of TGF-β1-mediated Smads/ERK signaling pathway[J].J Amry Med Univ (J Third Mil Med Univ),2017,39(05 ):442-447.DOI:
王芳芹, 刘涛, 张攀, et al. Astaxanthin inhibits lung fibrosis via down-regulation of TGF-β1-mediated Smads/ERK signaling pathway[J]. Journal of Army Medical University, 2017, 39(5): 442-447.DOI:
Astaxanthin inhibits lung fibrosis via down-regulation of TGF-β1-mediated Smads/ERK signaling pathway
Objective To determine the effect of astaxanthin (AX) on bleomycin (BLM)-induced lung fibrosis in SD rats and explore the underlying mechanism. Methods Thirty-two healthy male SD rats (weighing 200~220 g) were randomly divided into 4 groups
that is
Sham
BLM
AX
and AX+BLM groups. After intratracheal administration of BLM (5 mg/kg) or normal saline (Sham)
the rats were orally administered with AX (2 mg/kg) oil solution or vegetable oil daily for the AX group and AX+BLM group or BLM group respectively for 14 consecutive days. All rats were sacrificed in 24 h after the last administration and the lung tissues were harvested. Lung pathological changes were evaluated by lung coefficient calculation
hematoxylin-eosin staining
Masson trichrome staining and hydroxyproline assay. The expression of αSMA in the lung tissue was determined by immunohistochemical assay
and the serum level of TGFβ1 was measured by enzyme linked immunosorbent assay (ELISA). The expression of Smad2/3 and ERK1/2 in the lung tissues were determined by Western blotting. Results Compared with the Sham and AX groups
the BLM group showed severe lung injury
with obvious formation of lung fibrosis. But the AX+BLM group had notably alleviated lung inflammation and fibrosis (P0.01)
reduced collagen deposition
decreased hydroxyproline content (P0.01)
lower expression of α-SMA
declined level of TGF-β1 (P0.05)
and decreased expression levels of Smad2/3 and p-ERK1/2. Conclusion AX exerts obvious inhibitory effect on BLM-induced lung fibrosis
which may be related with its decreasing the TGF-β1 level and thus down-regulating Smads/ERK signaling pathway.