ArticleJournal of cellular and molecular medicine2019
5,2'-dibromo-2,4',5'-trihydroxydiphenylmethanone attenuates LPS-induced inflammation and ROS production in EA.hy926 cells via HMBOX1 induction.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Chrysotoxine Attenuates Key Atherogenic Processes via Antioxidant, Anti-Inflammatory, and COX-Dependent Antiplatelet Mechanisms.Biomolecules · 2026Article
- 5,2'-Dibromo-2,4',5'-trihydroxydiphenylmethanone Inhibits LPS-Induced Vascular Inflammation by Targeting the Cav1 Protein.Molecules (Basel, Switzerland) · 2022Article
- HMBOX1 attenuates LPS-induced periodontal ligament stem cell injury by inhibiting CXCL10 expression through the NF-κB signaling pathway.Experimental and therapeutic medicine · 2022Article
- Article
- GSK3β-dependent lysosome biogenesis: An effective pathway to mitigate renal fibrosis with LM49.Frontiers in pharmacology · 2022Article
- Review
- Process Development and Synthesis of Process-Related Impurities of an Efficient Scale-Up Preparation of 5,2'-Dibromo-2,4',5'-Trihydroxy Diphenylmethanone as a New Acute Pyelonephritis Candidate Drug.Molecules (Basel, Switzerland) · 2020Article
- 5,2'-dibromo-2,4',5'-trihydroxydiphenylmethanone attenuates LPS-induced inflammation and ROS production in EA.hy926 cells via HMBOX1 induction.Journal of cellular and molecular medicine · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
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Abstract
Inflammation and reactive oxygen species (ROS) are important factors in the pathogenesis of atherosclerosis (AS). 5,2'-dibromo-2,4',5'-trihydroxydiphenylmethanone (TDD), possess anti-atherogenic properties; however, its underlying mechanism of action remains unclear. Therefore, we sought to understand the therapeutic molecular mechanism of TDD in inflammatory response and oxidative stress in EA.hy926 cells. Microarray analysis revealed that the expression of homeobox containing 1 (HMBOX1) was dramatically upregulated in TDD-treated EA.hy926 cells. According to the gene ontology (GO) analysis of microarray data, TDD significantly influenced the response to lipopolysaccharide (LPS); it suppressed the LPS-induced adhesion of monocytes to EA.hy926 cells. Simultaneously, TDD dose-dependently inhibited the production or expression of IL-6, IL-1β, MCP-1, TNF-α, VCAM-1, ICAM-1 and E-selectin as well as ROS in LPS-stimulated EA.hy926 cells. HMBOX1 knockdown using RNA interference attenuated the anti-inflammatory and anti-oxidative effects of TDD. Furthermore, TDD inhibited LPS-induced NF-κB and MAPK activation in EA.hy926 cells, but this effect was abolished by HMBOX1 knockdown. Overall, these results demonstrate that TDD activates HMBOX1, which is an inducible protective mechanism that inhibits LPS-induced inflammation and ROS production in EA.hy926 cells by the subsequent inhibition of redox-sensitive NF-κB and MAPK activation. Our study suggested that TDD may be a potential novel agent for treating endothelial cells dysfunction in AS.
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