Effect of Budesonide on transform growth factor-β1 induced vascular endothelial growth factor release by lung fibroblasts
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Effect of Budesonide on transform growth factor-β1 induced vascular endothelial growth factor release by lung fibroblasts
Journal of Chongqing Medical UniversityVol. 37, Issue 8, Pages: 686-689(2012)
作者机构:
1. 重庆医科大学附属第一医院呼吸内科,重庆,400016
2. 四川大学华西医院生物治疗国家重点实验室呼吸病学研究室,成都,610100
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Published:2012,
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CHEN Yajuan, WEN Fuqiang, WANG Tao, et al. Effect of Budesonide on transform growth factor-β1 induced vascular endothelial growth factor release by lung fibroblasts. [J]. Journal of Chongqing Medical University 37(8):686-689(2012)
DOI:
CHEN Yajuan, WEN Fuqiang, WANG Tao, et al. Effect of Budesonide on transform growth factor-β1 induced vascular endothelial growth factor release by lung fibroblasts. [J]. Journal of Chongqing Medical University 37(8):686-689(2012)DOI:
Effect of Budesonide on transform growth factor-β1 induced vascular endothelial growth factor release by lung fibroblasts
Objective:To observe the effect of glucocorticoid(Budesonide) on TGF-β1 induced human fetal lung fibroblasts-1(HFL-1) secretion and vascular endothelial growth factor(VEGF) pro-duction and to discuss its mechanism. Methods:HFL-1 were cultured in vitro and were treated with various concentrations of Budesonide in the presence of TGF-β1 stimulation. Post-culture media were collected and VEGF content was tested by enzyme-linked immunosorbent(ELISA). The cell lysates were subjected to Western blot analysis to test the protein expressions of phosphor-ERK MAPK and phosphor-Smad3. Results:Budesonide can induce VEGF release by HFL-1 in a dose-dependent manner(P<0.05). Budesonide with high concentration can suppress the TGF-β1 induced VEGF release(P<0.05). The protein expressions of phosphor-ERK MAPK and phosphor-Smad3 were decreased after Budesonide pre-treatment(P<0.05). Conclusions:Budesonide may reduce TGF-β1 induced VEGF production in the lung,probably through the Smad/ERK signaling pathway,which may provide new sight into the molecular mechanism underlying glucocorticoids therapy for airway inflammatory diseases.