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benzydamine inhibits osteoclast differentiation and bone resorption via down-regulation of interleukin-1β expression

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Acta Pharmaceutica Sinica B 2020年第3期10卷 462-474页

作者： Han Saem Son Jiae Lee Hye In Lee Narae Kim You-Jin Jo Gong-Rak Lee Seong-Eun Hong Minjeong Kwon Nam Young Kim Hyun Jin Kim Jin Ha Park Soo Young Lee Woojin Jeong Department of Life Science and the Research Center for Cellular Homeostasis Ewha Womans UniversitySeoul 03760South Korea

Bone diseases such as osteoporosis and periodontitis are induced by excessive osteoclastic activity,which is closely associated with ***(BA)has been used as a cytokine-suppressive or non-steroidal anti-inflammatory drug that inhibits the production of proinflammatory cytokines or ***,its role in osteoclast differentiation and function remains ***,we explored the role of BA in regulating osteoclast differentiation and elucidated the underlying *** inhibited osteoclast differentiation and strongly suppressed interleukin-1β(IL-1β)*** inhibited osteoclast formation and bone resorption when added to bone marrowderived macrophages and differentiated osteoclasts,and the inhibitory effect was reversed by IL-1β*** reporter assay and the inhibitor study of IL-1βtranscription suggested that BA inhibited nuclear factor-κB and activator protein-1 by regulating IκB kinase,extracellular signal regulated kinase and P38,resulting in the down-regulation of IL-1β*** also promoted osteoblast ***,BA protected lipopolysaccharide-and ovariectomy-induced bone loss in mice,suggesting therapeutic potential against inflammation-induced bone diseases and postmenopausal osteoporosis.

关键词： benzydamine Osteoclast Bone Interleukin-1β Nuclear factor-κB Activator protein-1

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Repurposed benzydamine targeting CDK2 suppresses the growth of esophageal squamous cell carcinoma

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Frontiers of Medicine 2023年第2期17卷 290-303页

作者： Yubing Zhou Xinyu He Yanan Jiang Zitong Wang Yin Yu Wenjie Wu Chenyang Zhang Jincheng Li Yaping Guo Xinhuan Chen Zhicai Liu Jimin Zhao Kangdong Liu Zigang Dong The Pathophysiology Department School of Basic Medical SciencesAcademy of Medical SciencesZhengzhou UniversityZhengzhou 450000China The China-US(Henan)Hormel Cancer Institute Zhengzhou 450000China State Key Laboratory of Esophageal Cancer Prevention and Treatment Zhengzhou 450000China Provincial Cooperative Innovation Center for Cancer Chemoprevention Zhengzhou UniversityZhengzhou 450000China Cancer Chemoprevention International Collaboration Laboratory Zhengzhou 450000China Oncology Department The Tumor Hospital of Linzhou CityLinzhou 456500China

Esophageal squamous cell carcinoma (ESCC) is one of the leading causes of cancer death worldwide. It is urgent to develop new drugs to improve the prognosis of ESCC patients. Here, we found benzydamine, a locally acting non-steroidal anti-inflammatory drug, had potent cytotoxic effect on ESCC cells. benzydamine could suppress ESCC proliferation in vivo and in vitro. In terms of mechanism, CDK2 was identified as a target of benzydamine by molecular docking, pull-down assay and in vitro kinase assay. Specifically, benzydamine inhibited the growth of ESCC cells by inhibiting CDK2 activity and affecting downstream phosphorylation of MCM2, c-Myc and Rb, resulting in cell cycle arrest. Our study illustrates that benzydamine inhibits the growth of ESCC cells by downregulating the CDK2 pathway.

关键词： benzydamine cyclin-dependent kinase 2 patient-derived xenograft esophageal squamous cell carcinoma

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