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Diallyl disulfide inhibits proliferation and transdifferentiation of lung fibroblasts through induction of cyclooxygenase and synthesis of prostaglandin E-2
Wang, Yanhua1; Cao, Rong2; Wei, Bo1; Chai, Xiaoyu1; Sun, Dan1; Guan, Y.2; Liu, Xin-min1
关键词Diallyl Disulfide Cyclooxygenase Pge2 Fibrosis Histone Acetylation
刊名MOLECULAR AND CELLULAR BIOCHEMISTRY
2014-08-01
DOI10.1007/s11010-014-2048-9
393期:1-2页:77-87
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Cell Biology
研究领域[WOS]Cell Biology
关键词[WOS]IDIOPATHIC PULMONARY-FIBROSIS ; INCREASES HISTONE ACETYLATION ; NF-KAPPA-B ; NITRIC-OXIDE ; MYOFIBROBLAST DIFFERENTIATION ; STIMULATED MACROPHAGES ; GARLIC OIL ; CELL-LINES ; EXPRESSION ; MECHANISMS
英文摘要

Platelet-derived growth factor-BB (PDGF-BB) and transforming growth factor-beta 1 (TGF-beta 1) are critically involved in idiopathic pulmonary fibrosis by inducing the proliferation and transdifferentiation of lung fibroblasts. In the present study, we examined the impact of diallyl disulfide (DADS), a garlic-derived compound, on such pathological conditions. DADS showed profound inhibitory effects on the PDGF-BB-induced proliferation of human and mouse lung fibroblasts. DADS also abrogated the TGF-beta 1-induced expression of alpha-smooth muscle actin, type I collagen and fibronectin. Following treatment with DADS, the expression of cyclooxygenase-2 (COX-2) and the synthesis of prostaglandin E-2 (PGE(2)) were found to be markedly enhanced, which in turn led to elevated cAMP levels in lung fibroblasts. Notably, the effect of DADS was largely abolished in the presence of either COX inhibitor indomethacin or siRNA-targeting COX-2, or in the absence of the PGE(2) receptor EP2, supporting an essential role for the COX-2-PGE(2)-cAMP autocrine loop. Furthermore, we demonstrated that the upregulated expression of COX-2 was a result of increased level of histone 3 acetylation at COX-2 locus in DADS-treated cells. Together, these results suggest that DADS, by inducing COX-2 expression, may have therapeutic potential in treating lung fibrosis.

语种英语
WOS记录号WOS:000338348700009
项目编号81270114
资助机构National Natural Sciences Foundation of China
引用统计
被引频次:3[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/59813
专题北京大学第一临床医学院_老年病内科
作者单位1.Peking Univ, Dept Geriatr, Hosp 1, Beijing 100871, Peoples R China
2.Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Beijing 100871, Peoples R China
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GB/T 7714
Wang, Yanhua,Cao, Rong,Wei, Bo,et al. Diallyl disulfide inhibits proliferation and transdifferentiation of lung fibroblasts through induction of cyclooxygenase and synthesis of prostaglandin E-2[J]. MOLECULAR AND CELLULAR BIOCHEMISTRY,2014,393(1-2):77-87.
APA Wang, Yanhua.,Cao, Rong.,Wei, Bo.,Chai, Xiaoyu.,Sun, Dan.,...&Liu, Xin-min.(2014).Diallyl disulfide inhibits proliferation and transdifferentiation of lung fibroblasts through induction of cyclooxygenase and synthesis of prostaglandin E-2.MOLECULAR AND CELLULAR BIOCHEMISTRY,393(1-2),77-87.
MLA Wang, Yanhua,et al."Diallyl disulfide inhibits proliferation and transdifferentiation of lung fibroblasts through induction of cyclooxygenase and synthesis of prostaglandin E-2".MOLECULAR AND CELLULAR BIOCHEMISTRY 393.1-2(2014):77-87.
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