The present study investigated the effect of puerarin on promoting the osteogenesis in steroid-induced necrosis of the femoral head (SONFH). New Zealand rabbits were administrated with horse serum and methylprednisolone (MPS) for establishing SONFH in vivo model, which was then treated with puerarin treatment. Histo-morphological changes in the femoral head were examined by hematoxylin-eosin staining. Osteoblasts were isolated from healthy rabbits and treated by individual or combined administration of dexamethasone and puerarin. Osteoblast viability was measured by CCK-8 assay. Mineralized nodule formation was evaluated by alizarin red assay. Expressions of RUNX family transcription factor 2 (RUNX2), Type-I collagen α 1 (COL1A1), ALP and miR-34a in the femoral head were determined by qRT-PCR and Western blot. Puerarin attenuated the effect of SONFH on promoting histopathological abnormalities and counteracted SONFH inhibition on the expressions of ALP, RUNX2, COL1A1 and miR-34a in the rabbits. Rabbit osteoblasts were successfully isolated, as they showed red mineralized nodules. Dexamethasone exposure decreased osteoblast viability, which was increased by puerarin treatment. Furthermore, puerarin treatment attenuated dexamethasone-induced inhibition on the viability, osteoblastic differentiation, and the expressions of ALP, RUNX2, COL1A1 and miR-34a in the osteoblasts. Puerarin facilitated osteogenesis of steroid-induced necrosis of rabbit femoral head and osteogenesis of steroid-induced osteocytes via miR-34a upregulation.
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http://dx.doi.org/10.1016/j.cyto.2021.155512 | DOI Listing |
Animal Model Exp Med
December 2024
Orthopedic Center, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China.
Background: Zinc-finger E-box-binding homeobox-1 (ZEB1) is predominantly found in type-H vessels. However, the roles of ZEB1 and type-H vessels in steroid-induced osteonecrosis of the femoral head (SONFH) are unclear.
Methods: Human femoral heads were collected to detect the expression of ZEB1 and the levels of type-H vessels.
Small
November 2024
Department of Joint Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China.
Overproduction of reactive oxygen species (ROS) results in oxidative stress, a critical factor in the pathogenesis of steroid-induced osteonecrosis of the femoral head (SONFH). Excess ROS not only hinders the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) but also impairs mitochondrial structure and function, resulting in irreversible cellular damage. Herein, a biomimetic multifunctional scaffold comprising Zn-modified metal-organic framework 818 (Zn-MOF-818) loaded with deferoxamine (DFO), gelatin methacryloyl (GelMA) hydrogel, and demineralized bone matrix (DBM) is shown to scavenge excess ROS, promote angiogenesis, and regulate immunity.
View Article and Find Full Text PDFAnn Med
December 2024
Department of Orthopedics, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China.
Background: Osteonecrosis of the femoral head (ONFH) is a refractory orthopedic disease with a high disability rate. Long-term administration of steroids is the most common pathogenic factor for non-traumatic ONFH. Early diagnosis of steroid-induced osteonecrosis of the femoral head (SONFH) is difficult and mainly depends on imaging.
View Article and Find Full Text PDFJ Orthop Surg Res
October 2024
Department of Orthopedics Trauma and Microsurgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Chem Biol Interact
December 2024
Department of Joint Surgery, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, Shandong, 250021, China; Orthopaedic Research Laboratory, Medical Science and Technology Innovation Center, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, 250117, China; Department of Joint Surgery, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, 250012, China. Electronic address:
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