ObjectiveTo summarize the advance of triggering receptor expressed on myeloid cells-1 (TREM-1). MethodsLiteratures about the recent studies on the TREM-1 were reviewed. ResultsTREM1 was a mediator of inflammation. It could amplify the inflammation and lead to overexpression of inflammation in final. ConclusionTREM-1 is very important in development of many diseases and provide a new molecule target to cure.
Objective To investigate the inhibition effect of silence of a disintegrin and metalloproteinase 17 (ADAM17) gene on proliferation and apoptosis of HT29 colon cancer cells and its possible mechanism. Methods HT29cells were divided into 3 groups: cells of interference group were transfected with recombinant lentivirus vector, cells of negative control group were transfected with negative recombinant lentivirus vector, and cells of blank control group were treated with PBS. The expression of ADAM17 mRNA was detected by real-time PCR, the expressions of ADAM17 protein, caspase3, protein kinase B (Akt), glycogen synthase kinase-3β (GSK3β), phospho-protein kinase B (P-Akt), phospho-glycogen synthase kinase-3β (P-GSK3β) protein were detected by Western blot method, the cell proliferation was detected by MTT assay, and the apoptosis rate was detected by Annexin V-FITC/PI cell death detection kit. Results Compared with the control group and the negative control group, the interference group was related to low expressions of ADAM17 mRNA and its protein, low optical density value at the same time point (24, 48, and 72 h), high apoptosis rate, high expression level of caspase3 protein, but low expression levels of P-Akt and P-GSK3β protein (P<0.05). Conclusion Silent ADAM17 gene could significantly induces apoptosis and inhibits the proliferation of HT29 cells, which maybe via inhibiting Akt/GSK3β signaling pathway.
ObjectiveTo explore the protective effect of low-molecular-weight heparin calcium (LHC) combined with trimetazidine on intestinal smooth muscle of intestinal acute mesangial vein thrombosis (AMVT) in rats and it's mechanism of effect. MethodsA total of 120 SD male rats were randomly divided into three groups, with 40 rats in each group. LHC group: after the AMVT model established, rats were subcutaneous injection the LHC (30 U/100 g) per 12 h until 72 h after surgery. LHC+trimetazidine group (LHCT group): after the AMVT model established, rats were subcutaneous injection the LHC (30 U/100 g) and tail vein injection the trimetazidine (10 mg/kg) per 12 h until 72 h after surgery. Normal saline group (NS group): after the AMVT model established, rats were subcutaneous injection the NS (0.2 mL/100 g) per 12 h until 72 after surgery. The AMVT model were established by blocking superior mesenteric vein of 8 cm and the edge vein arch. Vena cava blood samples and intestinal segments were collected sequentially at 6 h, 12 h, 24 h, 48 h and 72 h afrer surgery. The levels of malondialdehyde (MDA) and creatine kinase (CK) in the blood, and the level of ATP in the intestinal tissue samples were measured with ELISA. Intestinal tissue were taken from the rats for inestinal tissue section, stained with hematoxylin and eosin, examined under light microscopy and evaluated histopathologically using mesemeche scoring system at different time. ResultsCompared with the LHC group and NS group, the levels of MDA and CK in blood and histopathology score of intestinal tissues in rats were significantly decreased, and the level of ATP significantly increased in LHCT group at different time point (P < 0.05). ConclusionTrimetazidine can improve intestinal smooth muscle energy metabolism in the AMVT disease, comined with LHC early can avoid intestinal smooth muscle wall permeability coagulation necrosis and reduce the intestinal smooth muscle damage.