ArticleInternational journal of molecular medicine2015
The thymoquinone-induced production of reactive oxygen species promotes dedifferentiation through the ERK pathway and inflammation through the p38 and PI3K pathways in rabbit articular chondrocytes.
Article in International journal of molecular medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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Who cites it
45 citing papers in PubMed, 84 citations in OpenAlex.
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- Oxidative Stress, MicroRNAs, and Long Non-Coding RNAs in Osteoarthritis Pathogenesis: Cross-Talk and Molecular Mechanisms Involved.International journal of molecular sciences · 2025Review
- Anti-Breast Cancer Effects of Thymoquinone-Chemotherapeutic Combinations: A Systematic Review of the LatestJournal of clinical medicine research · 2025Article
- Cisplatin-induced oxidative stress, apoptosis, and pro-inflammatory responses in chondrocytes through modulating LOX-1.Journal of orthopaedic surgery and research · 2025Article
- Targeted treatment of rat AKI induced by rhabdomyolysis using BMSC derived magnetic exosomes and its mechanism.Nanoscale advances · 2024Article
- Selenium Ameliorates Acetaminophen-Induced Oxidative Stress via MAPK and Nrf2 Pathways in Mice.Biological trace element research · 2024Article
- Novel insight on IRE1 in the regulation of chondrocyte dedifferentiation through ER stress independent pathway.Journal of physiology and biochemistry · 2024Article
- The Modulation of Phospho-Extracellular Signal-Regulated Kinase and Phospho-Protein Kinase B Signaling Pathways plus Activity of Macrophage-Stimulating Protein Contribute to the Protective Effect of Stachydrine on Acetaminophen-Induced Liver Injury.International journal of molecular sciences · 2024Article
- The research landscape of oxidative stress in osteoarthritis from 1998 to 2021: a systematic bibliometric analysis.American journal of translational research · 2024Article
- ERK/NF-kB/COX-2 Signaling Pathway Plays a Key Role in Curcumin Protection against Acetaminophen-Induced Liver Injury.Life (Basel, Switzerland) · 2023Article
- Celastrol-loaded biomimetic nanodrug ameliorates APAP-induced liver injury through modulating macrophage polarization.Journal of molecular medicine (Berlin, Germany) · 2023Article
- Antinociceptive Action of Thymoquinone-Loaded Liposomes in an In Vivo Model of Tendinopathy.Pharmaceutics · 2023Article
- Metal-Organic Framework Functionalized Bioceramic Scaffolds with Antioxidative Activity for Enhanced Osteochondral Regeneration.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- The healing effects of thymoquinone on experimentally induced traumatic tendinopathy in rabbits.Journal of orthopaedic surgery and research · 2023Article
- Article
- Natural compounds protect against the pathogenesis of osteoarthritis by mediating the NRF2/ARE signaling.Frontiers in pharmacology · 2023Review
- Suramin enhances chondrogenic properties by regulating the p67Bone & joint research · 2022Article
- Gastrodin Alleviates Acetaminophen-Induced Liver Injury in a Mouse Model Through Inhibiting MAPK and Enhancing Nrf2 Pathways.Inflammation · 2022Article
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2 authors at 1 institution in 1 country.
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Abstract
Dedifferentiation and inflammation are major features of cartilage degeneration during the pathogenesis of osteoarthritis (OA). Thymoquinone (TQ) is the major compound of black seed oil isolated from Nigella sativa with various beneficial or harmful effects on several diseases; however, its effects on the dedifferentiation and inflammation of chondrocytes have not yet been characterized. In the present study, we investigated whether TQ regulates the dedifferentiation and inflammation of rabbit articular chondrocytes, focusing on the production of reactive oxygen species (ROS) in rabbit articular chondrocytes. TQ induced the generation of ROS in a dose-dependent manner, as shown by staining with the fluorescent probe, 2'-7'-dichlorofluorescein diacetate. We confirmed that TQ induced dedifferentiation by measuring the loss of type II collagen and the reduction in chondroitin sulfate proteoglycan levels. TQ also caused inflammation by inducing the expression of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2). The antioxidant, N-acetyl cysteine (NAC), prevented the dedifferentiation and inflammation which was generated by the TQ-induced production of ROS. Furthermore, TQ caused a dose-dependent increase in p38, phosphorylated extracellular signal-regulated kinase (p-ERK) and phosphoinositide 3-kinase (PI3K) expression. NAC abrogated this effect and attenuated the dedifferentiation and inflammation which was generated by the TQ-induced production of ROS. To identify the ROS-regulated pathways, we treated the chondrocytes with the p38 inhibitor, SB203580, the MEK inhibitor, PD98059, and the PI3K inhibitor, LY294002. PD98059 inhibited the TQ-induced dedifferentiation and SB203580 and LY294002 prevented the TQ-induced inflammation. These findings suggest that the TQ-induced production of ROS causes dedifferentiation through the ERK pathway and inflammation through the PI3K and p38 pathways in rabbit articular chondrocytes.
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