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Objective To research the effect of pure interbody fusion and interbody cage fusion under minimally invasive transforaminal lumbar interbody fusion treat to single segment of lumbar disc herniation,analysis clinical value the two methods.Methods A total of 61 cases single segment lumbar disc herniation were treated with MIS-TLIF surgery,were divided into pure interbody fusion group (group A) and interbody fusion Cage group (group B) according to different fusion methods.Operative time,blood loss and postoperative drainage were recorded in two groups,the clinical efficacy were tested by using of visual analogue score (VAS),Japanese Orthopedic Association scores (JOA),Oswestry disability index (ODI) score and Macnab standard,the interbody fusion ability were evaluated by power lumbar X-ray film and CT 3D reconstruction.Results The gender,age,disease duration and disease segments in two gracps were not found statistically significant difference (P＞0.05).Also,two groups of patients,blood loss,postoperative drainage has no significant difference (P＞0.05).After the operation,the VAS score,ODI score,JOA score and Macnab criteria,the last follow-up of intervertebral fusion rate in in tuo groups were not found statistically significant difference (P＞0.05).While the operative time,postoperative disc height changes were found significant difference between two groups (P＜ 0.05).Conclusion MIS-TLIF simple fusion for lumbar disc herniation will be available with equal clinical efficacy fusion rate compared with cage fusion.
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Objective To study effect of a novel schiff base ruthenium coordination compound on cell proliferation and apoptosis of gastric cancer SGC-7901 cell.Method Gastric cancer SGC-7901 cell were divided into four groups according to different treatment of novel schiff base ruthenium coordination compound (concentration of 10, 30, 50μmol/L) and blank group with DMSO.Cell proliferation was detected by MTT assay, cell apoptosis and cell cycle were analysed by flow cytometry.ResuIts MTT results showed the inhibitory effect of novel schiff base ruthenium coordination compound on SGC-7901 cell enhanced with the increase of its concentration, and inhibitory rates were higher than that of blank group at 24, 48, 72 h.Flow cytometry results showed the apoptosis rate of novel ruthenium coordination compound groups of 10, 30, 50μmol/L were (17.64 ±1.21)%, (26.47 ± 0.61)%, (55.63 ±1.49)%, respectively, all higher than that of blank group (P<0.05).The cell proportion of G1 phase increased with the increasing of the novel schiff base ruthenium coordination.ConcIusion A novel schiff base ruthenium coordination compound could inhibit the growth of gastric cancer SGC-7901 cells, promote apoptosis and arrest gastric cancer SGC-7901 cells at G1.
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Objective To explore the inhibition of Zn(PMFPCl) 2 on HepG2 cells and its mechanism.Methods The HepG2 cells were divided into control group and experimental group of 10, 30 and 70 μmol/L.The cell proliferation was detected by MTT assay, cell apoptosis and cell cycle was analysed by flow cytometry, cellular morphological change was observed with inverted microscope and the expressions of apoptosis-regulated proteins of p53, p21, caspase-3, bax and bcl-2 in HepG2 cells were detected by Western blot.Results The inhibitory rates of experimental groups (10, 30, 70μmol/L) at 24, 48 and 72h were significantly higher than those of control group (P<0.05), and the highest one was 63.29% of 70 μmol/L Zn (PMFPCl)2at 72 h.The apoptosis rates of each experimental group at 48h was significantly higher than that of control group (P<0.05).The cells were induced a remarkable G1 arrest by Zn(PMFPCl) 2 which could inhibit proliferation.The number of adherent cells reduced and cells shrank, convex on cytomembrane surface appeared and the cells changed to round and were brighter.Western blot results showed that the protein levels of p53, p21, caspase-3 and bax increased and bcl-2 decreased with the Zn(PMFPCl)2concentration increasing (P<0.05).Conclusion Zn(PMFPCl)2 could inhibit the proliferation and promote apoptosis of HepG2 cells whose mechanisms are promotation of p53, p21, caspase-3 and bax expressions and inhibition of bcl-2 expression.