ABSTRACT
Objective To investigate the effect and mechanism of autophagy inhibited by Met/HGF passway in alleviating myocardial ischemia and reperfusion injury.Methods Lsolated cardiomyocytes of rats were divided into 5 groups:control group,ischemia and reperfusion (IR) group,Met-transfection group,Met siRNA-transfection group,Met-transfection and HGF activator group.Over or less expressions of Met were controlled by the method of transfection.Cell proteins were extracted after IR injury.The expression of cell protein such as met,HGF,AMPK,PI3K,autophagy-related protein LC3B,Beclin-1 and apoptosis-related protein Bcl-2 were detected by Western blot.Results Compared with control group,Western blot results showed that the expression of AMPK and PI3K increased significantly by the method of over expression of Met and activation of HGF,the expression of autophagy-related protein LC3B and Beclin-1 decreased significantly at the same time.However,it showed an opposite trend in IR group and Met siRNA-transfection group.Conclusion Activation of the Met/HGF signal pathway inhibits autophagy and attenuates myocardial ischemia-reperfusion injury.
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Objective To evaluate the correlation between seram interleukin-10 (IL-10) and testosterone with coronary heart disease (CHD). Methods 387 patients were divided into CHD group (n = 239) and control group ( n = 148 ) according to the results of coronary angiography. CHD patients were divided into subgroups accord-ing to the numbers, Gensini score of lesions in the coronary arteries and clinical severity ( statue of stable coronary artery disease, unstable angina or acute myocardial infarction). Serum IL-10 and testosterone levels were measured by ELASA. Logistic regression and partial correlation were used to evaluate the correlation of serum IL-10 and testoster-one with CHD. Results IL-10 was significantly lower in the CHD group than in the control group[ (39.08 ± 14.22) ng/L vs (49.27 ± 24.67)ng/L, P < 0. 001 ]. The partial correlation analysis results in subgroups showed that the correlation coefficient of IL-10 with number of lesions,gensini score and clinical severity of CHD was - 0.25, P < 0.001, -0.25 ,P <0.05 and -0.25 ,P <0.001 ,respectively. Serum testosterone had no difference in control group and CHD group (P >0.05 ). Logistic regression analysis found that only smoking (OR = 3.79,95% CI 2.09～ 6.84,P<0.01) ,diabetes mellitus (OR =2.48,95% CI 1.05 ～5.88,P <0. 05) ,apoB ( OR = 14.3,95% CI 4.29～46.61 ,P <0.01 ) and IL-10 ( OR =0.74,95%, CI 0.57～0.89 ,P <0.01 ) entered the model. Conclusions Serum IL-10 is not only significantly correlated with CHD but also with its severity. IL-10 is an independent pro-tective factor for CHD.
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Objective To explore the expression of peroxisome proliferator activated receptor? (PPAR?) and its roles in the differentiation of mesenchymal stem cells (MSCs) induced by 5 Azacytidine. Methods 5 Azacytidine was used to induce the differentiation of primary cultured mesenchymal stem cells. The eukaryotic expression plasmid vector pEGFP N1 PPAR? was transfected into MSCs with lipotransfection method followed by G418 selection. The expression levels of PPAR? mRNA were detected by RT PCR. Immunohistochemistry and Western blot were employed to study the protein expression of PPAR?. Lipid droplets in the cells were stained with Oil Red O. Results No expression of PPAR? mRNA was found in undifferentiated MSCs. After induction by 5 Azacytidine, partial MSCs expressed PPAR? and differentiated into lipoblasts. MSCs, transfected with pEGFP N1 PPAR?2, differentiated into adipocytes. Conclusion 5 Azacytidine can induce the differentiation of MSCs into myoblasts and lipoblasts, which may be related to the expression of PPAR?.