Ginkgo biloba extract ameliorates skin fibrosis in a bleomycin-induced mouse model of systemic sclerosis

被引:0
|
作者
Lee, Beomgu [1 ]
Roh, Jong Seong [2 ]
Jeong, Hoim [1 ]
Kim, Yerin [1 ]
Lee, Jihyeon [1 ]
Yun, Changun [1 ]
Park, Jiyoung [3 ]
Kim, Da-sol [4 ]
Lee, Jungsoo [4 ,5 ]
So, Min Wook [6 ]
Kim, Aran [7 ,8 ]
Sohn, Dong Hyun [1 ,5 ]
Lee, Seung-Geun [7 ,8 ]
机构
[1] Pusan Natl Univ, Sch Med, Dept Microbiol & Immunol, 49 Busandaehak Ro, Yangsan 50612, Gyeongsangnam D, South Korea
[2] Daegu Haany Univ, Coll Korean Med, Dept Herbal Prescript, Gyongsan, South Korea
[3] Ulsan Natl Inst Sci & Technol, Coll Informat & Biotechnol, Dept Biol Sci, Ulsan, South Korea
[4] Pusan Natl Univ, Yangsan Hosp, Dept Dermatol, Yangsan, South Korea
[5] Pusan Natl Univ, Yangsan Hosp, Res Inst Convergence Biomed Sci & Technol, Yangsan, South Korea
[6] Pusan Natl Univ, Dept Ophthalmol, Dept Internal Med, Div Rheumatol, Yangsan, South Korea
[7] Pusan Natl Univ, Pusan Natl Univ Hosp, Dept Internal Med, Div Rheumatol,Sch Med, 179 Gudeok Ro, Busan 49241, South Korea
[8] Pusan Natl Univ Hosp, Biomed Res Inst, Busan, South Korea
关键词
Systemic sclerosis (SSc); Ginkgo biloba extract (GBE); transforming growth factor (TGF)-beta; skin fibroblast; adipocyte-myofibroblast transition (AMT); PULMONARY-FIBROSIS; PATHOGENESIS; BETA; ATHEROSCLEROSIS; FIBROBLASTS; MECHANISMS; APOPTOSIS; ORIGIN; LUNG;
D O I
10.1080/19768354.2024.2337761
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Systemic sclerosis (SSc) is a chronic autoimmune disease characterized by skin and internal organ fibrosis and obliterative vasculopathy. Few effective treatments are currently available for fibrosis in SSc, therefore, demand persists for novel therapies. Although use of Ginkgo biloba extract (GBE) has been reported to improve blood circulation and alleviate liver and lung fibrosis, its effect on skin fibrosis in SSc remains unclear. In this study, the effects and underlying mechanisms of GBE on skin fibrosis in bleomycin (BLM)-induced mouse model of SSc was investigated. GBE significantly reduced dermal thickness and protein levels of profibrotic factors in the BLM-induced SSc mouse model. Moreover, GBE inhibited the gene expression of profibrotic factors, such as COL1A1, alpha-SMA, and connective tissue growth factor (CTGF), in fibroblasts by suppressing transforming growth factor (TGF)-beta signaling. Furthermore, GBE inhibited the transdifferentiation of adipocytes into myofibroblasts. Thus, our findings suggest that GBE is a promising therapeutic candidate for the treatment of SSc.
引用
收藏
页码:152 / 160
页数:9
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