ABSTRACT
BACKGROUND:Mechanical, inflammatory, and biochemical factors, particularly matrix metaloproteinases and reactive oxygen lead to chondrocyte degeneration in osteoarthritis. Curcumin has been shown to be a potent antioxidant; however, its protective effects against chondrocyte degeneration in osteoarthritis remain unclear. OBJECTIVE:To investigate the potential molecular mechanisms underlying the protective effects of curcumin on articular cartilage of osteoarthritis in rats. METHODS:A total of 30 Sprague-Dawley rats were used and randomly divided into model group (positive control,n=15) and normal group (negative control,n=15). Rat models of traumatic osteoarthritis were established, and then cartilage cels were isolated from articular cartilage and culturedin vitro. Chondrocytes were treated with curcumin (curcumin group) or PDTC (an inhibitor of nuclear factor-kappa B) for 24 hours. The expression level of nuclear factor-kappa B P65 in nucleus and cytoplasm in chondrocytes were determined by western blot assay and immunofluorescence. Moreover, mRNA expressions of type II colagen, matrix metaloproteinase-1 and -13 were analyzed using RT-qPCR. RESULTS AND CONCLUSION: Nuclear factor-kappa B P65 protein was mainly expressed in nucleus, but few in cytoplasm in positive control group; the reversed results were found in the curcumin group. Nuclear translocation of nuclear factor-kappa B P65 was observed mainly in nucleus in the positive control group; however, that was observed mainly in cytoplasm in the negative control, curcumin, and PDTC groups. Matrix metaloproteinase-1 and -13 mRNA expressions were significantly decreased, while type II colagen mRNA expression was significantly increased in the curcumin group compared with the positive control group. These findings indicated that curcumin protect chondrocytes against degeneration through inhibiting the activation of nuclear factor-kappa B signaling pathway, suppressing nuclear translocation of nuclear factor-kappa B P65 and inhibiting the expressions of matrix metaloproteinase-1 and -13, which are responsible for upregulation of type II colagen expression.
ABSTRACT
BACKGROUND:Intra-articular injection of sodium hyaluronate or dexamethasone can relieve pain and increase range of motion after traumatic arthritis. OBJECTIVE:To observe the effect of dexamethasone combined with sodium hyaluronate on traumatic arthritis of rat knees. METHODS:Forty-eight Sprague-Dawley rats were randomly divided into four groups. The anterior ligament of the left knee was resected and the medial meniscus was removed to establish models of traumatic arthritis in al the rats. After 3 weeks, the four groups were respectively injected dexamethasone+sodium hyaluronate (combined group), dexamethasone, sodium hyaluronate, and nothing (control group). After 4, 8, 12 weeks of injection, the samples were obtained for gross observation, anteroposterior and lateral X-ray films and hematoxylin-eosin staining. RESULTS AND CONCLUSION:At 12 weeks after injection, X-ray films showed that there was no stenosis in the combined group, mild stenosis in the dexamethasone and sodium hyaluronate groups, and obvious stenosis in the control group (indicating severe osteoarthritis);hematoxylin-eosin staining exhibited the fibrous cartilage-like tissue grew wel in the combined group, varying degrees of proliferation of fibrous cartilage-like cells were visible in the dexamethasone and sodium hyaluronate groups, and there was a smal amount of fibrosis in the control group. These findings suggest that the combination of dexamethasone and sodium hyaluronate can improve the cartilage repair and restore the joint function.
ABSTRACT
BACKGROUND:Mesenchymal stem cel s can differentiate into nerve cel s by chemical induction or co-culture method, but whether mesenchymal stem cel s co-cultured with Schwann cel s differentiate into neuronal-like cel s or Schwann-like cel s is stil controversial. OBJECTIVE:To explore the inductive role of Schwann cel s derived from rats in the differentiation of human umbilical cord mesenchymal stem cel s. METHODS:Cocultures of human umbilical cord mesenchymal stem cel s (1×109/L) and Schwann cel s (1×109/L) from neonatal rats were performed using transwel culture dishes. After 2 weeks of cocultures, morphology of the cultured human umbilical cord mesenchymal stem cel s was observed, and the phenotypic changes of cel s were also detected with immumocytochemistry techniques. RESULTS AND CONCLUSION:After 2 weeks of cocultures, some differentiated cel s showed neuron-like morphology, and expressed nestin, NF-200 andβ-III-tubulin, but did not express Schwann cel special marker S100 and oligodendrocytes special marker MAB1580. These findings indicate that human umbilical cord mesenchymal stem cel s can transdifferentiate into neuronal-like cel s by cocultures with rat’s Schwann cel s.
ABSTRACT
BACKGROUND:The bone metabolism of osteoarthritis is regulated by estrogen with osteoblasts, osteoclasts and cytokines, as wel as a number of regulatory pathways. OBJECTIVE:To describe the role of estrogen and estrogen-related compounds for joint protection, repair of bone and cartilage cells, and inhibition of synovitis in osteoarthritis. METHODS:Author researched PubMed, Embase, Elseveir database from 1992 to 2014, with the key words of“osteoarthritis, estrogens, matrix metal oproteinases, interleukins, tumor necrosis factor-alpha”. After the quality of the included studies was evaluation, valid data were extracted and analyzed. RESULTS AND CONCLUSION:Estrogen can increase the expression of osteoprotegerin and nuclear factor-κB factor ligands in osteoblasts, inhibit bone resorption, prevent the onset and progression of osteoarthritis. Estrogen upregulates anti-osteoclast cytokines, downregulates pro-osteoclast factors, and contribute to regulate bone metabolism of osteoarthritis patients through bone morphogenetic protein and Wnt signaling. Estrogen promotes the adrenal cortex secretion of glucocorticoids and indirectly inhibits the production of matrix metal oproteinases by the hypothalamus-hypophysis-adrenal gland axis. Exogenous estrogen inhibits bone resorption, which may help to delay the development of osteoarthritis. Estrogen and estrogen-related compounds may inhibit the cartilage loss caused by synovitis and inflammatory factors in the late stage of osteoarthritis.
ABSTRACT
BACKGROUND: A novel biodegradable Mg-Zn alloy is designed which the density and the Young's modulus are proximal to human bone. At the same time, it depletes the toxicity of aluminium and rare earth element in commercial magnesium alloys. OBJECTIVE: To observe the effect of Mg-Zn alloy (Mg-6%Zn) on the integrin βi expression of preosteoblasts MC3T3-E1. DESIGN, TIME AND SETTING: A contrast study was performed at the Central Laboratory of the Sixth People's Hospital Affiliated to Shanghai Jiao Tong University between March and May 2008. MATERIALS: The Mg-6% Zn was prepared by School of Materials Science and Engineering of Shanghai Jiao Tong University, which the density was 1.82 g/cm~3 and the Young's modulus was nearly 44 GPa. Poly-L-lactic acid (PLLA) was used as the controls. MC3T3-E1 cells were provided by Chinese Academy of Science Type Culture Collection. METHODS: The cell attachment was observed after cultured with Mg-Zn and PLLA at 2, 24 and 48 hours under scanning electron microscope; the integrin β1 mRNA expression of MC3T3-E1 cultured with Mg-Zn and PLLA was estimated by real-time fluorescent quantitative polymerase chain reaction (real-time PCR) at days 1, 3, 6, 9,12 and 15 after culture. MAIN OUTCOME MEASURES: The MC3T3-E1 cells attachment on the material surface and the integrin β1 mRNA expression. RESULTS: MC3T3-E1 cell adhesion was better on the Mg-Zn alloy surfaces than on the PLLA surface; The integrin (31 mRNA of osteoblasts on Mg-Zn kept on expressing during experiment and increased with time (P < 0.01), but there was no significantly difference between the two groups at the same time (P > 0.05). CONCLUSION: MC3T3-E1 cell adhesion is better on the Mg-Zn alloy surfaces than on the PLLA surface, but it is not mediated by inducing the integrin p1 mRNA expression.
ABSTRACT
Objective To investigate the degradation of dicalcium phosphate dehydrate-coated Mg-Zn alloy in vivo and bone formation. Methods Left femoral condyles were drilled in 72 New Zealand rabbits, and were randomly divided into experiment group (n＝24, implanted with dicalcium phosphate dehydrate-coated Mg-Zn alloy rods), Mg-Zn alloy control group (n＝24, implanted with Mg-Zn alloy rods) and poly-L-lactide acid rod group (n＝24, implanted with poly-L-lactide acid rods). Serum concentrations of Mg~(2+) were examined 1 d pre-operation, and 1 d, 1 week, 2 weeks, 5 weeks and 10 weeks post-operation in experiment group and Mg-Zn alloy control group. Operation sites were examined by X-rays at 3, 6, 12 and 18 weeks post-operation. After X-ray examination at each time point, 6 rabbits in each group were sacrificed, and subjected to histopathological observation of live and kidney tissues by HE staining. Tissues from condyles of femur were observed by HE staining and 2, 4, 6-trinitrophenol rosein staining, and mineral apposition rate of bone was calculated. Results There was no significant difference in the concentrations of serum Mg~(2+) at each time point between Mg-Zn alloy control group and experiment group (P>0.05). X-ray examination revealed gas emerged near the implants 3 weeks after surgery in Mg-Zn alloy control group. However, there was no obvious histological abnormality in liver and kidney tissues. The mineral apposition rate was higher and the degradation of material was lower in experiment group than those in the other two groups. Conclusion Dicalcium phosphate dehydrate-coated Mg-Zn alloy has a favourable biocompatibility, and degrades more slowly in vivo.