ArticleBioengineered2022
Fumitremorgin C alleviates advanced glycation end products (AGE)-induced chondrocyte inflammation and collagen II and aggrecan degradation through sirtuin-1 (SIRT1)/nuclear factor (NF)-κB/ mitogen-activated protein kinase (MAPK).
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 9 citations in OpenAlex.
- Evaluating the Genotoxicity and Mutagenicity of Food Contaminants: Acrylamide, Penitrem A, and 3-Acetyldeoxynivalenol in Individual and Combined Exposure In Vitro.Journal of applied toxicology : JAT · 2025Article
- c-Jun N-terminal kinase signaling in aging.Frontiers in aging neuroscience · 2024Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fumitremorgin C is a potent and selective inhibitor of the breast cancer resistance protein. This study aimed to explore the role of fumitremorgin C in osteoarthritis (OA) and disclose the underlying mechanism. The cell viability of AGE-treated SW1353 cells in the presence of fumitremorgin C was detected by Cell Counting Kit-8 (CCK-8) assay. The inflammation and extracellular matrix (ECM) deposition of AGE-induced SW1353 cells was respectively measured by enzyme linked immunosorbent assay (ELISA), immunofluorescence, and Western blot. The expression of SIRT1 and NF-KB/MAPK signal was examined by Western blot. After that, SIRT1 inhibitor EX527 was added to observe the mechanism of action of fumitremorgin C. Fumitremorgin C restored the cell viability of SW1353 cells injured by AGE. Furthermore, it alleviated inflammation and ECM degradation in AGE-induced SW1353 cell. The SIRT1 expression decreased by AGE was recovered upon fumitremorgin C to SW1353 cells. The ratio of phosphorylated p65 (p-p65) and p65, phosphorylated JNK (p-JNK) and JNK, and phosphorylated 38 (p-38) and 38 were increased by AGE treatment, which was recovered by fumitremorgin C addition. SIRT1 inhibitor EX527 reverts the repressive effects of fumitremorgin C on inflammation and ECM degradation in AGE-induced SW1353 cell. In conclusion, fumitremorgin C alleviates AGE-induced inflammation and the degradation of collagen II and aggrecan through SIRT1/NF-κB/MAPK, which reveals the underlying mechanism by which fumitremorgin C alleviates OA.
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