Magnoflorine ameliorates cartilage degradation in osteoarthritis through inhibition of mitochondrial reactive oxygen species-mediated activation of the NLRP3 inflammasome.
Yi Peng, Yue-Hui Huang, Xiao Luo, Mei-Chen Li, Qing-Qing Xiao, Lu Qiu, Qiang Fu
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引用次数: 0
Abstract
This study investigated the role of magnoflorine (MAG) on cartilage protection in osteoarthritis. In vitro studies showed that MAG decreased the expression of inflammatory factors and inhibited extracellular matrix degradation in lipopolysaccharide- and ATP-stimulated C28/I2 cells. Importantly, MAG reduced the levels of pyroptosis-related proteins, including NLRP3, ASC, cleaved-caspase 1, GSDMD-N, IL-18, and IL-1β. Mechanistically, MAG reduced mtROS production and inhibited the activation of the NF-κB signaling pathway. In vivo study demonstrated that sodium iodoacetate-induced cartilage degradation and inflammatory factor release were reversed by MAG. Overall, MAG could inhibit mtROS-mediated NLRP3 inflammasome activation by suppressing mitochondrial dysfunction to ameliorate osteoarthritis.
期刊介绍：
The Journal of Asian Natural Products Research (JANPR) publishes chemical and pharmaceutical studies in the English language in the field of natural product research on Asian ethnic medicine. The journal publishes work from scientists in Asian countries, e.g. China, Japan, Korea and India, including contributions from other countries concerning natural products of Asia. The journal is chemistry-orientated. Major fields covered are: isolation and structural elucidation of natural constituents (including those for non-medical uses), synthesis and transformation (including biosynthesis and biotransformation) of natural products, pharmacognosy, and allied topics. Biological evaluation of crude extracts are acceptable only as supporting data for pure isolates with well-characterized structures.
All published research articles in this journal have undergone rigorous peer review, based on initial editor screening and anonymized refereeing by at least two expert referees.
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