摘要
Objective To explore the pathogenesis of steroid-induced osteonecrosis of the femoral head(SONFH)and the mechanism of Traditional Chinese Medicine(TCM)-based prescription for"Bringing Blood Downward"targeting SONFH through the OPG/RANKL/RANK signaling pathway.Methods Fifty male SD rats were randomly divided into model group and control group.The rats in the model group were treated with LPS and methylprednisolone to build a SONFH model.After 6 weeks,two rats were randomly selected respectively from the two groups,and the SONFH model was confirmed by histomorphological examination under light microscopy.The rats in a low,medium and high dose treatment groups(group L,M,and H)were intragastrically administrated with the Prescription for"Bringing Blood Downward"at concentrations of 2.5/5/10 g/kg.While the rats in the model group and control group were intragastrically administrated with normal saline at a concentration of 5 g/(kg·d).The pathological changes and expression levels of OPG,TRAF-6,and RANKL in each group were examined 4 weeks later.Results Compared with the model group,chondrocytes and cell matrix of groups L,M and H were less reduced,osteoclastic absorption and trabecular structure were less destroyed and the cells were less adipose.The adipocyte density in the control group and each treatment group was significantly lower than that in the model group(P<0.01).In the control group,the bone marrow cavity area was smaller than that in the model group(P<0.05),but there was no significant difference between each dose treatment groups and the model group(P>0.05).The expression levels of OPG,RANKL,TRAF-6 and OPG/RANKL ratio in the control group and groups L,M and H were significantly lower than those in the control group(P<0.01).Conclusion The TCM-based prescription for"Bringing Blood Downward"works to treat SONFH byregulating the activity of osteoclasts and osteogenic differen-tiation process of osteoblasts,improving the microcirculation environment of the femoral head,and inducing the formation of trabecular bone through the OPG/RANKL/RANK signaling pathway.It functions with its multitargetsin diverse methods.
摘要
Objective To investigate the effects of interferon alpha?2b(IFNα?2b)on serum Hepcidin in hepatitis C patients and its mechanism. Methods Hepatitis C patients were divided evenly into treatment group and control group according to whether they had received treatment with IFNα?2b in the past 3 months. The serum hepci?din was compared between the two groups. HepG2 cells and LO2 cells were treated for 24 hours at varied levels of IFNα?2b(0,50,100,200,400μL)and real?time PCR was used to detect the hepcidin,interleukin?6(IL?6)and signal transduction and transcription activator 3(STAT3)mRNA expression of cells. The protein levels of STAT3 and phosphorylated STAT3(pSTAT3)were measured by Western blot. The changes of these indexes were observed with the gradual increase of IFNα?2b levels. Results Serum Hepcidin level in the treatment group was significantly lower than the control(P<0.05). IFNα?2b inhibited the Hepcidin mRNA in HepG2 cells and LO2 cells. pSTAT3 was significantly decreased with the increased levels of IFNα?2b(P<0.05),and the expression of IL?6 and STAT3 had no significant changes with the increase of IFNα?2b. Conclusion The serum Hepcidin levels can be decreased because IFNα?2b suppresses the expression of Hepcidin,and its mechanism may be related with inhibited STAT3 pathway activation.
摘要
Objective To investigate the influence of miR-106b on Wnt/β-catenin pathway in HCC cells. Methods QGY-7703 and HepG2 cells were transfected with miRNA mimics or inhibitors. TOP/FOP luciferase ratio assay was used to test the Wnt/β-catenin pathway activity. The expression of downstream targeted genes of Wnt/β-catenin pathway were examined by Real-time PCR. The accumulation of β-catenin in nuclears were measured by Western blotting. Results Ectopic expression of miR-106b dramatically increased the average TOP/FOP ratio and the mRNA expression of downstream targeted genes in QGY-7703 and HepG2 cells. Compared with that in control cells , miR-106b over-expression promoted the nuclear β-catenin accumulation in QGY-7703 cells. Clonclusion MiR-106b activated Wnt/β-catenin pathway in HCC cells.