ArticleImmunity, inflammation and disease2024
The Nrf2/HO-1 pathway participates in the antiapoptotic and anti-inflammatory effects of platelet-rich plasma in the treatment of osteoarthritis.
Article in Immunity, inflammation and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Combined PRP and CCP Therapy Suppresses Inflammation and Protects Cartilage in Post-Traumatic Osteoarthritis.Veterinary sciences · 2026Article
- The Nrf2/HO-1 signaling pathway in arthritis: from molecular mechanisms to therapeutic potential.Frontiers in cell and developmental biology · 2026Review
- Platelet-rich plasma in cartilage repair: biological mechanisms and clinical perspectives.Frontiers in sports and active living · 2026Review
- The Nrf2/HO-1 pathway participates in the antiapoptotic and anti-inflammatory effects of platelet-rich plasma in the treatment of osteoarthritis.Immunity, inflammation and disease · 2024Article
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Authors and funding
4 authors.
Funding
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Abstract
introductionWe aimed to explore the molecular mechanisms through which platelet-rich plasma (PRP) attenuates osteoarthritis (OA)-induced pain, apoptosis, and inflammation.
methodsAn in vivo model of OA was established by injuring rats using the anterior cruciate ligament transection method, whereas an in vitro model was generated by exposing chondrocytes to interleukin (IL)-1β. Both models were then treated with PRP.
resultsIn both the in vivo and in vitro models, OA led to the suppression of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway, whereas treatment with PRP reactivated this molecular axis. Inhibition of the Nrf2/HO-1 pathway using the Nrf2 inhibitor brusatol or through Nrf2 gene silencing counteracted the effects of PRP in reducing the tenderness and thermal pain thresholds of OA rats. Additionally, PRP reduced the mRNA expression of IL-1β, IL-6, tumor necrosis factor-alpha (TNF-α), and matrix metallopeptidase 13 (MMP-13) and the protein expression of B-cell lymphoma 2 (Bcl-2), Bcl-2 associated X-protein (Bax), and caspase-3. Furthermore, inflammation and apoptosis were induced by brusatol treatment or Nrf2 silencing. Additionally, in the in vitro model, PRP treatment increased the proliferation of chondrocytes and attenuated their inflammatory response and apoptosis, effects that were abrogated by Nrf2 depletion.
conclusionsThe Nrf2/HO-1 pathway participates in the PRP-mediated attenuation of OA development by suppressing inflammation and apoptosis.
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