Open AccessAstragalus polysaccharide ameliorates steroid‐induced osteonecrosis of femoral head through miR ‐206/ HIF ‐1α/ BNIP3 axis
Author(s) -
Zhang ShenYao,
Wang Fan,
Zeng XiangJing,
Huang Zhen,
Dong KeFang
Publication year - 2021
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1002/kjm2.12426
Subject(s) - autophagy , apoptosis , gene knockdown , flow cytometry , microbiology and biotechnology , cell , downregulation and upregulation , western blot , microrna , cell growth , chemistry , biology , biochemistry , gene
Declining autophagy and rising apoptosis are the main factors driving the development of steroid‐induced osteonecrosis of the femoral head (SONFH). Here, we showed that astragalus polysaccharide (APS) improved femoral head necrosis via regulation of cell autophagy and apoptosis through microRNA (miR)‐206/hypoxia inducible factor‐1 (HIF‐1α)/BCL2 interacting protein 3 (BNIP3) axis. The expression of miR‐206, HIF‐1α, and BNIP3 in SONFH specimens and cell model were measured using qPCR. SONFH cell model was treated with APS. Cell autophagy was evaluated using LC3‐immunofluorescence assays. Flow cytometry was conducted to assess cell apoptosis. Apoptosis‐related proteins and autophagy‐related proteins were determined using western blot. Besides, dual‐luciferase reporter assay was employed to investigate the relationship between miR‐206 and HIF‐1α. Here we showed that miR‐206 expression was upregulated in SONFH tissues and cell model. APS promoted autophagy and inhibited apoptosis in SONFH cell model via downregulating miR‐206. What is more, HIF‐1α was the target of miR‐206. Knockdown of HIF‐1α reversed the recovery effect of miR‐206 inhibitor on SONFH cell model. Furthermore, BNIP3 was the target of HIF‐1α. HIF‐1α overexpression promoted autophagy and inhibited apoptosis, and knockdown of BNIP3 abolished the recovery effect of HIF‐1α overexpression in SONFH cell model. These results provided evidence that APS reduced miR‐206 expression, and the downregulated miR‐206 increased BNIP3 expression by targeting HIF‐1α to promote autophagy and inhibit bone cell apoptosis. Our research proved that APS effectively improved SONFH by regulating cell autophagy and apoptosis.