ArticleJournal of molecular histology2026
Alpha-2-macroglobulin attenuates glucocorticoid-induced osteonecrosis of the femoral head by enhancing osteogenesis and antioxidant defense via the Akt/Nrf2 signaling pathway.
Article in Journal of molecular histology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Glucocorticoid-induced osteonecrosis of the femoral head (GIONFH) is featured by oxidative stress and impaired bone regeneration. Alpha-2-Macroglobulin (α-2 M) was reported to possess cytoprotective and anti-inflammatory properties, and have shown its role in alleviating GIONFH. nuclear factor erythroid 2-related factor 2 (Nrf2) was proved to mediate oxidative stress in GIONFH. We aimed to investigate whether α-2 M attenuates GIONFH by exerting a dual osteogenic and antioxidant effect through the Akt/Nrf2 signaling pathway. We induced GIONFH model in rats and injected α-2 M and Nrf2 inhibitor subsequently. Micro-CT and histology revealed that α-2 M treatment prevented methylprednisolone (MPS)-induced bone loss, preserving trabecular structure and reducing empty lacunae. α-2 M reversed the MPS-mediated suppression of Akt-Nrf2 pathway, upregulating the expression of heme oxygenase-1 (HO-1) and osteogenic markers. The Nrf2 inhibitor ML385 negated these benefits, confirming that α-2 M mitigates GIONFH by upregulating osteogenesis and reducing oxidative stress through the Akt/Nrf2 axis. The results demonstrated that α-2 M is a promising target for managing GIONFH.
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