Identification of JUN as determinant of osteoarthritis and its inhibition by the Chinese herbal formulae Zhuanggu Huoxue Tang

Zheng, Zhenyu; Guo, Malong; Zhu, Wenxiao; Chen, Weidong; Kong, Liang; Liu, Yonghui; Qiu, Yue; Wang, Xiangyang; Wang, Yidi; Cui, Hongxun

doi:10.1016/j.compbiomed.2022.105786

Cited by 2 publications

(2 citation statements)

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Section: Introductionmentioning

confidence: 99%

“…2,3 The pathogenesis of OA is highly complex, and existing therapeutic interventions for OA primarily focus on alleviating symptoms rather than providing safe and effective medications for delaying or reversing the progression of the disease. 4 Ferroptosis is a unique form of cell death characterized by irondependent mechanisms, inactivation of glutathione peroxidase 4 (GPX4), and accumulation of lipid peroxides. 5,6 Unlike apoptosis, autophagy, necroptosis, and other forms of cell death, ferroptosis plays a role in the pathogenesis of various diseases, including tumors, 7 ischemic organ injury, 8 neurodegenerative disorders, 9 1 The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu, China hematological diseases, 10 and kidney injury.…”

Section: Introductionmentioning

confidence: 99%

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Quercetin Suppresses Ferroptosis in Chondrocytes via Activating the Nrf2/ GPX4 Signaling Pathway

Xu,

Lu,

Fang

et al. 2023

Natural Product Communications

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Background: Osteoarthritis is a progressive chronic disease that lacks effective treatment strategies. Ferroptosis features may be involved in the development and progression of osteoarthritis. Quercetin, a widely studied flavonoid compound, is considered a potential candidate for osteoarthritis therapies, although its anti-ferroptosis effect remains uncertain. This research aimed to investigate the regulatory impact of quercetin on ferroptosis and Nrf2 signaling in RSL3-induced C28/I2 cells. Methods: Cell viability was measured using the CCK-8 assay. Cellular lipid reactive oxygen species (ROS) were detected using fluorescence microscopy and flow cytometry combined with C11-BODIPY 581/591 staining. The level of malondialdehyde (MDA) was measured using an MDA assay kit. The level of GPX4 protein was determined by immunofluorescence staining and Western blotting. The protein levels of nuclear-Nrf2 and HO-1 were confirmed using Western blotting. Results: Quercetin improved cell viability, reduced the accumulation of lipid ROS, decreased MDA levels, elevated the protein levels of GPX4 and HO-1, and enhanced nuclear-Nrf2 protein levels in the ferroptosis cell model induced by RSL3. Additionally, the Nrf2 agonist TBHQ reversed ferroptosis in chondrocytes by activating the Nrf2/HO-1 pathway, while the Nrf2 inhibitor ML385 failed to protect against RSL3-induced ferroptosis in chondrocytes. Conclusion: Quercetin suppresses RSL3-induced ferroptosis in chondrocytes by activating the Nrf2/GPX4 signaling pathway, providing a promising therapeutic option for osteoarthritis.

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Section: Introductionmentioning

confidence: 99%