BackgroundThis study aimed to investigate the therapeutic effect of low, medium, and high concentrations of medical ozone on trauma-induced lumbar disc herniation.Material/MethodsA total of 80 patients were included and were grouped into a control group, a low medical ozone (20 μg/ml) group, a medium medical ozone (40 μg/ml) group, and a high medical ozone (60 μg/ml) group. The CT scan and enzyme-linked immunosorbent assay (ELISA) were used to detect IL-6 level, SOD activity, IgM, and IgG levels upon admission and at 6 and 12 months after follow-up. The area under the ROC curve (AUC) was calculated for visual analogue scale (VAS) and efficiency rate.ResultsAll patients showed disc retraction at 6- and 12-month follow-up; while patients in the medium medical ozone (40 μg/ml) group showed the greatest disc retraction rate. The IL-6, IgM, IgG, and VAS levels significantly decreased while SOD activity increased among all groups over time (p<0.05). The AUCIL-6, AUCIgG, AUCIgM, and AUCSOD was closest to 1 in the medium medical ozone (40 μg/ml) group compared with other groups (p<0.01), with the highest efficacy at 6 (35%) and 12 (85%) months during follow-up.ConclusionsLow concentrations of medical ozone (20 μg/ml and 40 μg/ml) reduced the serum IL-6, IgG, and IgM expression, presenting as analgesic and anti-inflammatory effects, while high concentrations of medical ozone (60 μg/ml) increased the serum IL-6, IgG, IgM expression, presenting as pain and pro-inflammatory effects.The medical ozone concentration of 40 μg/ml showed the optimal treatment efficacy.

Alendronate is commonly used for the treatment of postmenopausal osteoporosis; however, the underlying pathological molecular mechanisms of its action remain unclear. In the present study, the alendronate-treated signaling pathway in bone metabolism in rats with ovariectomy induced by osteoporosis was investigated. Rats with osteoporosis were orally administered alendronate or phosphate-buffered saline (control). In addition, the interferon-β (IFN-β)/signal transducer and activator of transcription 1 (STAT1) signaling pathway was investigated in osteoblasts following treatment with alendronate in vitro and in vivo. During the differentiation period, IFN-β (100 ng/ml) was used to treat the osteoblast cells, and the activity, viability and bone metabolism-associated gene expression levels (STAT1, p-STAT1, Fra1, TRAF6 and SOCS1) were analyzed in osteoblast cells. Histopathological changes were used to evaluate osteoblasts, osteoclasts, inflammatory phase of bone healing and osteonecrotic areas. The results demonstrated that alendronate significantly inhibited the activity of osteoporotic osteoclasts by stimulating expression of IFN-β, as well as markedly improved the viability and activity of osteoblasts compared with the control group. In addition, alendronate increased the expression and phosphorylation levels of STAT1 in osteoclasts, enhanced osteoblast differentiation, upregulated the expression levels of alkaline phosphatase and osteocalcin, and increased the expression of osteoblast differentiation-associated genes (osteocalcin, osterix and Runx2). Inhibition of IFN-β expression canceled the benefits of alendronate-mediated osteoblast differentiation. Notably, alendronate enhanced bone formation in rats with osteoporosis induced by ovariectomy. In conclusion, these findings suggest that alendronate can regulate osteoblast differentiation and bone formation in rats with osteoporosis induced by ovariectomy through upregulation of IFN-β/STAT1 signaling pathway.

Background: Spinal cord injury (SCI) is a destructive trauma accompanying with local injury, half of which cause chronic paralysis. Ginsenoside Rg1 exerts anti-apoptosis and anti-autophagy properties. Therefore, our goal was to study the protective mechanism of Rg1 in attenuating cell injury. Methods: MiR-216a-5p inhibitor was transfected into PC-12 cells, then cells were pre-treated by Rg1 and treated with 300 μ M hydrogen peroxide (H 2 O 2 ) for 24 h. CCK-8 and apoptosis experiments were done to test cell activity and apoptosis respectively. Expression of miR-216a-5p and cell damage relative factors was tested via qRT-PCR and western blot experiments, respectively. Results: H 2 O 2 induced cell activity suppression, apoptosis and autophagy well at the concentration of 300 μ M, leading cell injury. Rg1 could attenuate cell injury induced by H 2 O 2 at the working concentration of 200 μ M that it elevated cell activity, attenuated apoptosis and autophagy and activated PI3K/AKT and AMPK signal pathways. Further, miR-216a-5p was up-regulated by Rg1. Rg1 played its role in relieving cell injury by positively regulating miR-216a-5p. Conclusion:Our study demonstrated that Rg1 attenuated H 2 O 2 -caused cell injury through positively regulated miR-216a-5p.

BackgroundSpinal cord injury (SCI) is a destructive trauma accompanying with local injury, half of which cause chronic paralysis. Ginsenoside Rg1 exerts anti-apoptosis and anti-autophagy properties. Therefore, our goal was to study the protective mechanism of Rg1 in attenuating cell injury.MethodsMiR-216a-5p inhibitor was transfected into PC-12 cells, then cells were pre-treated by Rg1 and treated with 300 μM hydrogen peroxide (H2O2) for 24 h. CCK-8 and apoptosis experiments were done to test cell activity and apoptosis respectively. Expression of miR-216a-5p and cell damage relative factors was tested via qRT-PCR and western blot experiments, respectively.ResultsH2O2 induced cell activity suppression, apoptosis and autophagy well at the concentration of 300 μM, leading cell injury. Rg1 could attenuate cell injury induced by H2O2 at the working concentration of 200 μM that it elevated cell activity, attenuated apoptosis and autophagy and activated PI3K/AKT and AMPK signal pathways. Further, miR-216a-5p was up-regulated by Rg1. Rg1 played its role in relieving cell injury by positively regulating miR-216a-5p.ConclusionOur study demonstrated that Rg1 attenuated H2O2-caused cell injury through positively regulated miR-216a-5p.

ZrO2 was coated on AZ31 magnesium alloy substrate by plasma electrolytic oxidation with K2ZrF6 and NaH2PO4 electrolytes. The discharge characteristics and variation in active species during the plasma electrolytic oxidation (PEO) process were studied by optical emission spectroscopy. The surface morphology and element composition of the membranes were observed by scanning electron microscope. The ion transfer of the substrate was studied by atomic absorption spectroscopy. The phase composition and corrosion characteristics of the PEO membranes were examined with XRD and an electrochemical workstation, respectively. The heat and mass transfer models during the PEO process were introduced. The contributions of ions to the membranes and active species were also analyzed. The results indicated that the ion transfer at different stages exhibits different tendencies. At the first and transition stages, the migration resistance of the ions was low and increased gradually. At the initial discharge stage, the migration resistance was the highest because the highest membrane growth rate occurred at this stage. At the later discharge stage, the migration resistance tends to be stable, which is ascribed to a dynamic equilibrium PEO membrane growth rate. The intensity of active species is related to the energy state of the working electrode’s surface. The higher the energy, the greater the probability that the active species will be excited to generate energy level transitions, and the higher the plasma concentration.