Yue-Wen Chang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Yue-Wen Chang has a total of 6 co-authors. Here are the top co-authors by number of shared publications:
Hong-Sheng Zhan
Department of Orthopedics and Traumatology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
2 shared publicationsJian Pang
Department of Orthopedics and Traumatology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
2 shared publicationsWei Gu
Department of Orthopedics and Traumatology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
2 shared publicationsYue-Long Cao
Department of Orthopedics and Traumatology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
2 shared publicationsYong-Fang Zhao
Department of Orthopedics and Traumatology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China
1 shared publication- Yong-Fang Zhao
Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine
1 shared publication
Latest Publications
- RetractionOpen Access
- 18 February 2023
- Published by Springer Nature in Inflammation
- Vol. 46 (3) , 1131
Retraction Note: Bufalin Exerts Inhibitory Effects on IL-1β-Mediated Proliferation and Induces Apoptosis in Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes
- 18 February 2023
- Published by Springer Nature in Inflammation
- Vol. 46 (3) , 1131
RetractionOpen AccessRetraction Note: Bufalin Exerts Inhibitory Effects on IL-1β-Mediated Proliferation and Induces Apoptosis in Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes
- Retracted
- 22 April 2014
- Published by Springer Nature in Inflammation
- Vol. 37 (5) , 1552-1559
RETRACTED ARTICLE: Bufalin Exerts Inhibitory Effects on IL-1β-Mediated Proliferation and Induces Apoptosis in Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes
Rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) proliferate abnormally and resist apoptosis. Bufalin inhibits cell proliferation and induces apoptosis in human cancer cells. In this study, we explored the effects of bufalin on interleukin-1beta (IL-1β)-induced proliferation and apoptosis of RAFLSs. The cell proliferation and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay and annexin V/propidium iodide staining, respectively. Bufalin dose-dependently inhibited IL-1β-induced RAFLS proliferation. Mechanistically, bufalin decreased the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB), both of which are involved in IL-1β-mediated RAFLS proliferation. Moreover, bufalin induced apoptosis and mitochondrial damage of RAFLSs, which was associated with Bcl-2 downregulation, Bax upregulation, mitochondrial cytochrome c release, and enhanced cleavages of caspase-3 and poly-(ADP-ribose) polymerase. Collectively, our results reveal that bufalin suppresses IL-1β-induced proliferation of RAFLSs through MAPK and NF-κB signaling pathways and induces RAFLS apoptosis via the mitochondria-dependent pathway.
- 22 April 2014
- Published by Springer Nature in Inflammation
- Vol. 37 (5) , 1552-1559
RetractedRETRACTED ARTICLE: Bufalin Exerts Inhibitory Effects on IL-1β-Mediated Proliferation and Induces Apoptosis in Human Rheumatoid Arthritis Fibroblast-Like Synoviocytes
Rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) proliferate abnormally and resist apoptosis. Bufalin inhibits cell proliferation and induces apoptosis in human cancer cells. In this study, we explored the effects of bufalin on interleukin-1beta (IL-1β)-induced proliferation and apoptosis of RAFLSs. The cell proliferation and apoptosis were measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazoliumbromide assay and annexin V/propidium iodide staining, respectively. Bufalin dose-dependently inhibited IL-1β-induced RAFLS proliferation. Mechanistically, bufalin decreased the activation of mitogen-activated protein kinases (MAPKs) and nuclear factor-kappa B (NF-κB), both of which are involved in IL-1β-mediated RAFLS proliferation. Moreover, bufalin induced apoptosis and mitochondrial damage of RAFLSs, which was associated with Bcl-2 downregulation, Bax upregulation, mitochondrial cytochrome c release, and enhanced cleavages of caspase-3 and poly-(ADP-ribose) polymerase. Collectively, our results reveal that bufalin suppresses IL-1β-induced proliferation of RAFLSs through MAPK and NF-κB signaling pathways and induces RAFLS apoptosis via the mitochondria-dependent pathway.