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To observe the lesion characteristics of vertebral subchondral bone by establishing a rat model of intervertebral disc degeneration. Thirty-two Sprague--Dawley rats were randomly divided into four groups of eight rats each, and one group served as the control group without any treatment. The rats in the experimental group were injected with 30 μl of anhydrous alcohol under the endplate (sub-endplate) above the Co6 vertebrae and 30 μl of phosphate buffered saline buffer under the endplate above the Co8 vertebrae. Eight rats were randomly taken for follow-up testing at 2, 4, and 8 w after establishment of models. The rats underwent imaging X-rays and magnetic resonance imaging to assess vertebral subchondral bone and intervertebral disc degeneration grades; then serum enzyme-linked immunosorbent assay was performed to measure tumor necrosis factoralpha, interleukin-1 beta, type I procollagen amino-terminal peptide, type I collagen carboxy-terminal peptide, vascular endothelial growth factor A and endostatin. The Co5/Co6 and Co7/Co8 motion segments (including the adjacent vertebrae and intervertebral disc) were used to perform micro-computed tomography, histological staining with hematoxylin and eosin, sapphire green, and toluidine blue, as well as for detecting the expression of collagen type II, and vascular endothelial growth factor A expression. Collagen type II, aggregated proteoglycan (aggrecan), sox-9, vascular endothelial growth factor A by immunohistochemical tests. Imaging, histologic staining and immunohistochemistry confirmed the successful establishment of intervertebral disc degeneration model. Histological observations and immunohistochemical analysis showed progressive degeneration of major intervertebral disc structures. Blocking the intervertebral disc trophic pathway in the vertebral subchondral bone region can successfully establish intervertebral disc degeneration rat model, and the possible main lesion characteristics of the vertebral subchondral bone during this process include abnormal bone remodeling, destruction of blood vessels and enhanced inflammatory response. [ABSTRACT FROM AUTHOR]

Introduction. This study aimed to investigate the effects of stromal cell-derived factor-1 (SDF-1) and activation of its receptor, chemokine receptor 4 (CXCR4), on the osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs), and the key signaling mechanisms involved in these effects. Material and methods. BMSCs were treated with 100 μg/L SDF-1 and cultured in osteogenic medium for 7 days. RT-qPCR and western blotting were used to detect the protein and mRNA levels of Janus kinase 2 (JAK2), signal transducer and activator of transcription 3 (STAT3), Runt-related transcription factor 2 (Runx2), and osteocalcin (OCN). Alizarin-red staining was used to detect the mineralization-inducing ability of the cells. Results. After BMSCs were treated with SDF-1, the levels of JAK2 mRNA, STAT3 mRNA, and protein phosphorylation increased, the number of mineralized nodules of BMSCs increased, and the osteogenic-differentiation ability was enhanced. In addition, after BMSCs were treated with an inhibitor of JAK2 phosphorylation, the levels of JAK2, STAT3, Runx2, and OCN decreased significantly, the number of mineralized nodules of BMSCs also decreased, and the osteogenic-differentiation ability decreased. The inhibition of CXCR4-treated BMSCs further confirmed that SDF-1/CXCR4 activated JAK2/STAT3 to regulate the osteogenic differentiation of BMSCs. Conclusions. SDF-1/CXCR4 promoted the osteogenic differentiation of BMSCs through JAK2/STAT3 activation. [ABSTRACT FROM AUTHOR]

Nerve conduits have emerged as alternatives to autologous nerve grafts, but their use in large-diameter, critical nerve repairs is limited. In the previous study, we prepared a PRGD/PDLLA/β-TCP/NGF sustained-release nerve conduit, which was made of RGD peptide modified poly[(lactic acid)-co-[(glycolic acid)-alt-(L-lysine)]] (PRGD), poly(d,l-lactic acid) (PDLLA), β-tricalcium phosphate (β-TCP) and nerve growth factor (NGF). Here we attempted to use the PRGD/PDLLA/β-TCP/NGF sustained-release nerve conduit to bridge a 30-mmdog tibial nerve defect in six beagles. The other beagles were divided into group autograft (n = 6) as positive control and group PDLLA (n = 6) as negative control. After 9 months of implantation, nerve conduction velocities, the density of myelinated fibers, the mean diameter of axon, and the average thickness of myelin sheath in tibial nerves bridged with PRGD/PDLLA/β-TCP/NGF sustained-release nerve conduits were similar to those treated with autologous nerve (p > 0.05). Neither electrophysiological nor histological restoration was obtained in group PDLLA. Evidence is thus provided in support of the use of PRGD/PDLLA/β-TCP/NGF sustained-release nerve conduits as alternatives to autologous nerve grafts for treatment of largediameter, critical defects in peripheral nerves. [ABSTRACT FROM AUTHOR]