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Osteoarthritis (OA) is a prevalent bone and joint disease characterized by degeneration. The dysregulation between chondrocyte synthesis and breakdown is a key factor in OA development. Targeting the degenerative changes in cartilage tissue degradation could be a potential treatment approach for OA. Previous research has established a strong link between autophagy and the regulation of chondrocyte functions. Activating autophagy has shown promise in mitigating cartilage tissue degeneration. Currently, osteoarthritis treatment primarily focuses on symptom management, as there is no definitive medication to stop disease progression. Previous studies have demonstrated that luteolin, a flavonoid present in Chinese herbal medicine, can activate autophagy and reduce the expression of MMP1 and ADAMTS-5. This study utilized an in vitro osteoarthritis model with chondrocytes stimulated by IL-1β, treated with varying concentrations of luteolin. Treatment with luteolin notably increased the levels of synthesis factors Aggrecan and Collagen II, while decreasing the levels of decomposition factors MMP-1 and ADAMTS-5. Moreover, inhibition of autophagy by Chloroquine reversed the imbalances in chondrocyte activities induced by IL-1β. In an in vivo model of knee osteoarthritis induced by medial meniscal instability (DMM), luteolin was administered as a therapeutic regimen. After 12 weeks, knee cartilage tissues from mice were analyzed. Immunofluorescence and immunohistochemical staining revealed a decrease in P62 expression and an increase in Beclin-1 in the cartilage tissues. Additionally, cartilage wear in the knee joints of mice was alleviated by safranin O and fast green staining. Our study findings underscore the significant role of luteolin in effectively rebalancing chondrocyte activities disrupted by IL-1β. Our results strongly indicate that luteolin has the potential to be developed as a novel therapeutic agent for the treatment of osteoarthritis, offering promising prospects for future drug development.
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http://dx.doi.org/10.1016/j.heliyon.2024.e31028 | DOI Listing |
Adv Sci (Weinh)
September 2025
State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University, Yangling, Shaanxi, 712100, P. R. China.
Mounting evidence indicates that viruses exploit elevated reactive oxygen species (ROS) levels to promote replication and pathogenesis, yet the mechanistic underpinnings of this viral strategy remain elusive for many viral systems. This study uncovers a sophisticated viral counter-defense mechanism in the Cryphonectria hypovirus 1 (CHV1)-Fusarium graminearum system, where the viral p29 protein subverts host redox homeostasis to overcome antiviral responses. That p29 directly interacts with and inhibits the enzymatic activity of fungal NAD(P)H-dependent FMN reductase 1 (FMR1), leading to increased ROS accumulation and subsequent autophagy activation is demonstrated.
View Article and Find Full Text PDFBrain
September 2025
Okinawa Institute of Science and Technology Graduate University, Okinawa, 904-0495, Japan.
Animal models of the pathology of Parkinson's disease (PD) have provided most of the treatments to date, but the disease is restricted to human patients. In vitro models using human pluripotent stem cells (hPSCs)-derived neural organoids have provided improved access to study PD etiology. This study established a method to generate human striatal-midbrain assembloids (hSMAs) from hPSCs for modeling alpha-synuclein (α-syn) propagation and recapitulating basal ganglia circuits, including nigrostriatal and striatonigral pathways.
View Article and Find Full Text PDFAdv Sci (Weinh)
September 2025
Department of Occupational Health (Key Laboratory of Electromagnetic Radiation Protection, Ministry of Education), Army Medical University (Third Military Medical University), Chongqing, 400038, China.
Cadmium (Cd) is a heavy metal that exhibits strong carcinogenic properties and promotes breast cancer (BC) progression. Autophagic flux dysfunction is involved in Cd-induced BC progression, but the underlying molecular mechanisms remain unclear. Here, it is observed that impaired autophagic flux and metabolic reprogramming are notable features related to Cd-induced proliferation, migration, and invasion in BC cell lines, including T-47D and MCF-7 cells.
View Article and Find Full Text PDFFront Mol Biosci
August 2025
Department of Neurosurgery, Jiangnan University Medical Center, Wuxi, Jiangsu, China.
Introduction: Sulforaphane (SFN) is recognized for its anti-inflammatory properties; however, the underlying molecular mechanisms remain unclear. In this study, we explored the effect of SFN on subarachnoid hemorrhage (SAH) and the potential mechanisms.
Methods: Sprague-Dawley (SD) rats were divided into three groups (n = 12): Sham + vehicle group (Sham + V), SAH + vehicle group (SAH + V), and SAH + SFN group (SAH + S).
Diabetes Metab Syndr Obes
September 2025
Medical School, Kunming University of Science and Technology, Kunming, People's Republic of China.
Diabetes has emerged as a critical global health issue, with its associated complications posing a severe threat to patients' quality of life. Current research demonstrates that imbalance in mitochondrial dynamics and autophagic dysregulation play pivotal roles in the pathogenesis of diabetic complications, particularly in diabetic cardiomyopathy, nephropathy, peripheral neuropathy and retinopathy. Strategic modulation of mitochondrial function and autophagic activity represents a promising therapeutic approach for managing diabetic complications.
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