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Impaired autophagy and mitochondrial dysfunction further accelerate disc degeneration. Pure platelet-rich plasma (P-PRP), enriched in growth factors and low in pro-inflammatory mediators, has shown regenerative potential. However, its mechanism of action, particularly the role of the autophagy-related SIRT1 pathway and mitochondrial homeostasis, remains unclear.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods<\/jats:title>\n            <jats:p>Rabbit-derived P-PRP was prepared and analyzed for cellular content and cytokine profiling. NPCs were treated with whole blood or P-PRP, and assessed for viability (CCK-8) and migration (Transwell). An IL-1\u03b2-induced degeneration model was established, and groups were treated with SIRT1 activator (SRT1720), inhibitor (EX527), P-PRP, or P-PRP\u2009+\u2009EX527. Mitochondrial membrane potential (JC-1 staining), and apoptosis (Annexin V\/PI flow cytometry) were also measured. Western blotting, immunofluorescence, qPCR, and ELISA were conducted to measure the expression of SIRT1, autophagy-related proteins, and ECM-related markers.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Results<\/jats:title>\n            <jats:p>P-PRP promoted the viability and migration of NPCs, reduced apoptosis, and preserved ECM homeostasis in inflammatory conditions. P-PRP enhanced the expression of SIRT1, improved mitochondrial membrane potential, and reduced apoptosis rates. P-PRP upregulated LC3B-II and Beclin-1 expression, while downregulated p62 expression, indicating autophagy activation. EX-527 abrogated the beneficial effects of P-PRP.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion<\/jats:title>\n            <jats:p>P-PRP protected against degenerative NPCs by activating functional autophagic flux and restoring mitochondrial function via the SIRT1 signaling axis. These findings provide novel mechanistic insight into PRP-based therapies and identify SIRT1 as a promising target for the treatment of IVDD.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1186\/s13018-025-06205-0","type":"journal-article","created":{"date-parts":[[2025,8,22]],"date-time":"2025-08-22T10:26:24Z","timestamp":1755858384000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Pure platelet-rich plasma delays intervertebral disc degeneration by activating SIRT1-mediated autophagy in nucleus pulposus cells"],"prefix":"10.1186","volume":"20","author":[{"given":"Jiaheng","family":"Han","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Zhili","family":"Ding","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jie","family":"Huang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yan","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yu","family":"Ding","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"297","published-online":{"date-parts":[[2025,8,22]]},"reference":[{"issue":"6","key":"6205_CR1","doi-asserted-by":"publisher","first-page":"e316","DOI":"10.1016\/S2665-9913(23)00098-X","volume":"5","author":"regional Global","year":"2023","unstructured":"Global regional, national burden of low back pain. 1990\u20132020, its attributable risk factors, and projections to 2050: a systematic analysis of the global burden of disease study 2021. 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