Objective To evaluate the clinical efficacy of salmeterol /fluticasone propionate in the treatment of chronic obstructive pulmonary disease .Methods 107 patients with chronic obstructive pulmonary disease from June 2012 to June 2014 were randomly divided into control group and observation group .Patients in control group re-ceived routine therapy, yet patients in observation group received salmeterol /fluticasone propionate on the basis of routine therapy.The st.George respiratory questionnaire (SGRQ) mark, 6 -minwalktest (6MWT),pulmonary func-tion indexes and drug adverse reactions before treatment and after treatment were observed respectively .Results Af-ter treatment, the lung function index recovery , the SGRQ total score,6MWT of observation group was obviously bet -ter than that of the control group , and the difference had statistical significance (p <0.05).There were no serious adverse reactions occurred in the two groups , and with no statistically significant difference (p >0.05).Conclusion On top of conventional therapy ,salmeterol /fluticasone propionate has good clinical curative effect and high safety for treating COPD,and so it is suitable for long -term and sustained treatment .

Objective To study the effect of matrine on ATP binding cassette transporter A1 (ABCA1) expression and cholesterol in monocyte derived foam cells. Methods The lipid peroxide in cells was measured by TBARS method; The foam cells were examined by oil red O stain. The accumulation of cholesterol in monocyte was measured by fluorescence spectrophotometric method;ABCA1 mRNA and its protein level were determined by RT-PCR and Western blot, respectively. Results In the homonocytes incubated with PMA and low density lipoprotein (LDL), the intracellular accumulated total cholesterol (TC), free cholesterol (FC), cholesteryl ester (CE) and lipid peroxide increased obviously, and a huge amount of foam cells were found by oil red O stain. This was accompanied by a reduction in the membrane content of ABCA1. matrine alter ABCA1 mRNA abundance, indicating that increased ABCA1 transcription, enhanced mRNA level.Conclusion The mechanism of anti-artherosclerosis by matrine may be related to reduce cholesterol and to increase the level of ABCA1 expression.

AIM:To study the role of prostaglandin F2?(PGF2?) in cardiac hypertrophy and its relation with calcineurin(CaN) signal transduction pathway in vitro.METHODS:The cultured neonatal rat cardiomyocyte was used to observe the hypertrophic effect of PGF2?,and the hypertrophic response was assayed by measuring the cell diameter,protein content and atrial natriuretic factor(ANF) mRNA expression.For mechanism studies,the intracellular free calcium concentration([Ca2+]i) in cultured cardiomyocytes was measured by using Fura-2/AM as a fluorescent indicator.ANF and CaN mRNA expressions,and the expressions of CaN and its downstream effectors,NFAT3 and GATA4 proteins were assayed by RT-PCR and Western blotting,respectively.RESULTS:In cultured cardiomyocytes,PGF2? induced profound hypertrophic morphology change and the significant increase in cell diameter,and protein content in a concentration-dependent manner compared with those in vehicle control(P

Aim To explore the effect of miRNA-143 ( miR-1 4 3 ) on homocysteine ( Hcy ) induced-vascular smooth muscle cells ( VSMCs ) proliferation and the mechanism .Methods VSMCs were cultured and in-cubated with Hcy by using primary cultured method . Then, cells were treated with different concentrations of Hcy and folate .VSMCs proliferation was determined with MTT assay , miR-143 was measured by qRT-PCR, and methylation of miR-143 was determined with meth-ylated PCR.Results After cells were treated with dif-ferent concentrations of Hcy , the proliferation of VSMCs was significantly increased , mRNA expression of miR-143 was decreased and methylation of miR-143 was increased .The proliferation of VSMCs was signifi-cantly decreased when transfected VSMCs with miR-143 precursor , and cell proliferation was increased by using miR-143 inhibitor transfection .Conclusion Hy-pomethylation of miR-143 may inhibit VSMCs prolifera-tion.