ArticleMolecular medicine reports2022
Tetramethylpyrazine alleviates endoplasmic reticulum stress‑activated apoptosis and related inflammation in chondrocytes.
Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Heat shock proteins in osteoarthritis: molecular mechanisms, pathogenic roles, and therapeutic opportunities.Frontiers in immunology · 2025Review
- Integration of Network Pharmacology, Molecular Docking, and Experimental Validation to Identify the Effect of EGCG on Alleviating Chondrocyte Inflammatory Damage by Targeting ER Stress-STAT3 Crosstalk.Journal of inflammation research · 2025Article
- Programmed Cell Death of Chondrocytes, Synovial Cells, Osteoclasts, and Subchondral Bone Cells in Osteoarthritis.Journal of inflammation research · 2025Review
- Article
- Endoplasmic reticulum stress-mediated apoptosis and autophagy in osteoarthritis: From molecular mechanisms to therapeutic applications.Cell stress & chaperones · 2024Review
- Nutritional Epigenomics: Bioactive Dietary Compounds in the Epigenetic Regulation of Osteoarthritis.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Tetramethylpyrazine alleviates hypoxia-induced proliferation, migration, and inflammatory response of fibroblast-like synoviocytes via inhibiting the HIF-1α- circCDC42BPB pathway.Advances in rheumatology (London, England) · 2024Article
- Tetramethylpyrazine inhibits ferroptosis in spinal cord injury by regulating iron metabolism through the NRF2/ARE pathway.Frontiers in pharmacology · 2024Article
- Recent Therapeutic Strategies for Excessive Chondrocyte Death in Osteoarthritis: A Review.Orthopaedic surgery · 2023Review
- Role of signal transduction pathways in IL-1β-induced apoptosis: Pathological and therapeutic aspects.Immunity, inflammation and disease · 2023Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Excessive apoptosis of chondrocytes and degradation of the extracellular matrix (ECM) contribute to the typical pathological characteristics of osteoarthritis (OA). Various studies have reported that tetramethylpyrazine (TMP) protects against multiple disorders by inhibiting inflammation and oxidative stress. The present study investigated the effects of TMP on chondrocytes and evaluated the associated mechanisms. To determine the effect of TMP on OA and the underlying mechanisms, chondrocytes were incubated with TMP and IL‑1β or thapsigargin (TG) Western blotting assays were performed to examine the expression levels of endoplasmic reticulum (ER) stress proteins, and TUNEL staining, fluorescence immunostaining and reverse transcription‑quantitative PCR were used to determine the apoptosis levels, and catabolic and inflammatory factors. It was found that TMP protected chondrocytes by suppressing IL‑1β‑induced expression of glucose‑regulated protein 78 (GRP78) and CHOP (an apoptotic protein). TMP regulated the TG‑mediated upregulated expression of GRP78 and CHOP in the chondrocytes of rats, as well as markedly suppressed levels of ER stress‑triggered inflammatory cytokines (TNF‑α and IL‑6). Furthermore, TMP modulated TG‑induced changes in ECM catabolic metabolism in rat chondrocytes. Collectively, TMP alleviated ER‑stress‑activated apoptosis and related inflammation in chondrocytes, indicating that it has therapeutic potential for the treatment of OA.
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