{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T18:59:30Z","timestamp":1791313170433,"version":"4.3.1"},"reference-count":48,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2024,6,11]],"date-time":"2024-06-11T00:00:00Z","timestamp":1718064000000},"content-version":"vor","delay-in-days":10,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunity Inflam &amp;amp; Disease"],"published-print":{"date-parts":[[2024,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:sec><jats:title>Introduction<\/jats:title><jats:p>We aimed to explore the molecular mechanisms through which platelet\u2010rich plasma (PRP) attenuates osteoarthritis (OA)\u2010induced pain, apoptosis, and inflammation.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>An 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)\u20101\u03b2. Both models were then treated with PRP.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In both the in vivo and in vitro models, OA led to the suppression of the nuclear factor erythroid 2\u2010related factor 2 (Nrf2)\/heme oxygenase\u20101 (HO\u20101) pathway, whereas treatment with PRP reactivated this molecular axis. Inhibition of the Nrf2\/HO\u20101 pathway using the Nrf2 inhibitor brusatol or through <jats:italic>Nrf2<\/jats:italic> 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 <jats:italic>IL\u20101\u03b2<\/jats:italic>, <jats:italic>IL\u20106<\/jats:italic>, tumor necrosis factor\u2010alpha (<jats:italic>TNF\u2010\u03b1<\/jats:italic>), and matrix metallopeptidase 13 (<jats:italic>MMP\u201013<\/jats:italic>) and the protein expression of B\u2010cell lymphoma 2 (Bcl\u20102), Bcl\u20102 associated X\u2010protein (Bax), and caspase\u20103. Furthermore, inflammation and apoptosis were induced by brusatol treatment or <jats:italic>Nrf2<\/jats:italic> 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.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>The Nrf2\/HO\u20101 pathway participates in the PRP\u2010mediated attenuation of OA development by suppressing inflammation and apoptosis.<\/jats:p><\/jats:sec>","DOI":"10.1002\/iid3.1169","type":"journal-article","created":{"date-parts":[[2024,6,11]],"date-time":"2024-06-11T18:47:58Z","timestamp":1718131678000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["The Nrf2\/HO\u20101 pathway participates in the antiapoptotic and anti\u2010inflammatory effects of platelet\u2010rich plasma in the treatment of 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