Objective:To investigate the effect of atorvastatin on the blood lipid and uric acid levels of elderly patients with coronary heart disease complicated with diabetes mellitus.Methods:116 patients with coronary heart disease and diabetes were randomly divided into the control group and the experimental group,58 cases in each group.Both groups of patients were given blood glucose control,blood pressure and other symptomatic treatment.The control group was treated with Aspirin Enteric-coated Tablets 0.3～0.6 g/times,3 times/d,oral,clopidogrel tablets,2 tablets each time,1 time/d,oral,nitroglycerin,0.25～0.5 g/time,3 times/d,with service;the experimental group was given atorvastatin on the basis of control group,10～20 mg/time,1 time/d,treatment for 4 weeks.During the treatment,the dosage was timely adjusted according to the conditions of patients.The serum low density lipoprotein cholesterol (LDL-C),high density lipoprotein cholesterol (HDL-C),triglyceride (TG),total cholesterol (TC),uric acid (UA),glycosylated hemoglobin (HbA1c) levels before and after treatment and the clinical treatment efficiency were observed and compared between two groups.Results:Compared with before treatment,the serum LDL-C,TG,TC,UA,HbA1c levels were decreased ahter treatment in both groups of patients,the HDL-C level was increased (P＜0.05);compared with the control group,the serum LDL-C,TG,TC,UA,HbA1c levels were lower,HDL-C level was higher in the experimental group (P＜0.05);compared with the control group,the effective rate of clinical treatment of the experimental group were higher (P＜0.05).Conclusion:Atorvastatin could effectively reduce the blood glucose,blood lipid,uric acid levels of elderly patients with coronary heart disease complicated with diabetes.

Objective To construct the has-miR 146a eukaryotic overexpression vector pmR 146a and to explore its effect on the expression of c-Myc gene in HepG2.2.15 cells.Methods The has-miR-146a precursor gene fragment pre-has-miR-146a was amplified by PCR,then connected to the pmR-mCherry plasmid vector after double enzyme digestion,the accuracy of recombinant vector was verified by colony PCR,double enzyme digestion and sequencing;then the recombinant vector was transfected into HepG2.2.15 cells as the experimental group,meanwhile the empty vector group (transfecting pmR-mCherry empty plasmid group) and blank group(transfecting reagent lip2000+PBS),then the fluorescent protein expression amount was observed under the fluorescence microscopy at 24,48 h;the expression of has miR-146a was evaluated by qPCR;at 24,48 h after transfection,the expression levels of c-Myc gene mRNA were detected by qPCR,and the c-Myc protein expression level after 48 h was detected by Western blot.Results The colony PCR,double enzyme digestion and sequencing verified that the pre-has-miR-146a gene fragment was inserted into the pmR-mCherry vector;at 24,48 h after transfection in the experimental group and empty vector group,intracellular strong fluorescence was seen by fluorescent microscope,the transfection efficiency was at 50％-60％ contrasting without fluorescence;the has-miR-146a expression level in the experimental group was significantly higher than that in the empty vector group and blank group (P＜0.01);the c-Myc mRNA expression at 24,48 h after tranfection was significantly lower than that in the empty vector group and blank group (P＜0.05);the protein expression amount at 48 h after transfection was lower than that in the empty vector group and blank group (P＜0.01).Conclusion The pmR-146a eukaryotic overexpression vector is successfully constructed,this recombinant vector can express miR-146a stably;miR-146a can down-regulate c-Myc cancer gene expression,which can serve as one of potential targets for treating hepatocellular carcinoma.

Objective: To construct the mmu-miR-155 eukaryotic overexpression vector pmR-155 and to investigate its effect on HBV replication and expression of PTEN in vivo. Methods: The mmu-mir-146a precursor gene fragment pre-mmu-mir-146a was amplified by PCR, then connected to the pmR-mCherry plasmid vector after double enzyme digestion, the accuracy of recombinant vector was verified by colony PCR、double enzyme digestion and sequencing; then the recombinant vector was transfected HBV transgene mice(Experimental Group)with hydrodynamics-based injection via vena caudalis, and pmR-mCherry plasmid、PBS were respectively transfected into the mice as Empty plasmid Group、Blank Group. The concentration of IFN-γ in the serum was detected by ELISA. The expression of SOCS1、PTEN mRNA in the liver was detected by qPCR at 30d post-transfectioned. The Western blot was performed to detect the changes in SOCS1、PTEN、HBX in the liver tissue at 30 d post-transfectioned. The results were analyzed with Student’s t-test, or one-way analysis of variance and the least significant difference test. Results: the colony PCR、double enzyme digestion and sequencing verified that the gene was inserted into the pmR-mCherry vector. Compared with Blank Group, the expression of miR-155 in the Experimental Group was significantly increased(t = 8.90, P < 0.01); the concentration of IFN-γ in the Experimental Group was significantly increased(F = 26.58, P < 0.01); the mRNA(F_{SOCS1 mRNA} = 19.72, P < 0.01; F_{PTEN mRNA} = 7.38, P < 0.05) and protein(F_SOCS1 = 50.30, P < 0.01; F_PTEN = 129.00, P < 0.01) expression of COCS1、PTEN was significantly decreased in the Experimental group and the protein of HBX was also significantly(F_HBX = 77.97, P < 0.01). Conclusion The pmR-155 eukaryotic overexpression vector is successfully constructed, this recombinant vector can express miR-155 stably; miR-155 can down-regulate cocs1、PTEN gene expression and up-regulate the expression of IFN-γ, it can inhibit the replication of HBV and a potential targets to treating hepatocellular carcinoma.