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MC3T3-E1 cells were exposed to DEX at different concentrations (0, 10<jats:sup>\u22128<\/jats:sup>, 10<jats:sup>\u22127<\/jats:sup>, 10<jats:sup>\u22126<\/jats:sup>, 10<jats:sup>\u22125<\/jats:sup> and 10<jats:sup>\u22124<\/jats:sup>\u00a0mol\/L), and cell viability, flow cytometry and TUNEL assay were used to detect cell proliferation and apoptosis. An FGF-2-pcDNA3 plasmid (oe-FGF-2) was used to overexpress FGF-2, and western blotting was conducted to detect protein expression.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Results<\/jats:title>\n                <jats:p>We found that FGF-2 was downregulated in the DEX-treated group. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated that DEGs were associated with PI3K\/Akt signaling pathway. DEX downregulated FGF-2 gene and protein expression, inhibited viability and induced MC3T3-E1 cell apoptosis. Overexpression of FGF-2 reversed DEX-induced apoptosis in MC3T3-E1 cells. FGF-2-mediated anti-apoptosis was impaired by inactivating the PI3K\/AKT pathway with LY294002. Moreover, overexpression of FGF2 delayed the progression of DEX-induced osteonecrosis of the femoral head (ONFH) animal model by regulation PI3K\/Akt signaling pathway.<\/jats:p>\n              <\/jats:sec><jats:sec>\n                <jats:title>Conclusion<\/jats:title>\n                <jats:p>In conclusion, FGF-2 is effective at inhibiting DEX-induced MC3T3-E1 cell apoptosis through regulating PI3K\/Akt signaling pathway.<\/jats:p>\n              <\/jats:sec>","DOI":"10.1186\/s13018-021-02715-9","type":"journal-article","created":{"date-parts":[[2021,10,18]],"date-time":"2021-10-18T17:32:12Z","timestamp":1634578332000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Overexpression of FGF2 delays the progression of osteonecrosis of the femoral head activating the PI3K\/Akt signaling pathway"],"prefix":"10.1186","volume":"16","author":[{"given":"Pei","family":"Lu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi-min","family":"Shen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ting","family":"Hua","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ting","family":"Pan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gang","family":"Chen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Teng","family":"Dai","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ke-qin","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,10,18]]},"reference":[{"key":"2715_CR1","doi-asserted-by":"publisher","first-page":"2982480","DOI":"10.1155\/2020\/2982480","volume":"2020","author":"M Huang","year":"2020","unstructured":"Huang M, Wang Y, Peng R. 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