ABSTRACT
Objective: To explore the correlation of monocyte to HDL-C ratio (MHR) and post-operative slow lfow or no relfow in patients with ST-segment elevation myocardial infarction (STEMI) after percutaneous coronary intervention (PCI). Methods: A total of 216 STEMI patients treated in our hospital from 2014-10 to 2016-05 were enrolled. The patients were divided into 2 groups: Slow lfow or no relfow group, the patients with TIMI grade≤2,n=43 and Normal lfow group, n=173. Receiver operating characteristic (ROC) curve was performed to assess the best cut-off value for MHR predicting slow lfow or no relfow with its sensitivity and speciifcity; Logistic regression analysis was conducted to studied weather MHR could be used as an independent risk factor for coronary slow lfow or no relfow in STEMI patients after PCI. Results: Compared with Normal lfow group, Slow lfow or no relfow group had the higher MHR (18.6±9.8) vs (10.9±5.5), P<0.001. Univariate Regression analysis indicated that MHR was a risk factor of slow lfow or no relfow occurrence (OR=2.22, 95% CI 1.58-3.28); multivariate regression analysis presented that MHR was an independent risk factor of slow lfow or no relfow occurrence (OR=1.55, 95% CI 1.01-2.38). ROC curve showed that the best cut-off value for MHR predicting slow lfow or no relfow occurrence was 13.37 with the sensitivity and speciifcity at 67.4% and 70.5% respectively, the area under curve (AUC) was 0.734, 95% CI 0.646-0.822. Conclusion: MHR was an independent risk factor for slow lfow or no relfow occurrence in STEMI patients after PCI.
ABSTRACT
Objective To study the effect of Cardiotrophin-1 (CT-1) on cardiocyte hypoxia-reoxygenation injury,and to investigate the signaling pathways involved in the protective effect. Method This study was carried out in Key Lab of Molecular Medicine in Jiangxi Province. Cardiomyocytes from the hearts of 2-day-old Sprague-Dawley neonatal rats were prepared by a modified method. Five groups were included in the study. Group (ⅰ): control, Group (ⅱ): hypoxia/reoxygeuation, Group (ⅲ): hypoxia / reoxygenation + CT-1, Group (iv) : CT- 1 + hypoxia/ reoxygenation + LY294002 (PIK3/Akt inhibitor), Group (ⅴ): CT-1 + hypoxia / reoxygenation +DMSO. The concentration of CT-1 was 10 ng/mL. Myocytes survival rote was evaluated by MTS method, apopto-sis, mitochondrial permeability transition pore (△ψm) and reactive oxygen species(ROS) were detected by flow cy-tometer, phosphorylased GSK-3β and PI3K protein by western blotting. Analysis of variance and q test as statistical methods was used to analyze the data. Results Cardiomyocyte apoptosis and ROS increased markedly after hy-poxia/reoxygenation,but cardiomyocyte survival rate and the level of △ψm [(40.55±4.25) vs. (86.28±7.15), P < 0.01]decreased significantly. With CT-1 intervention, cardiomyocyte survival rate increased markedly (87%),apoptosis and ROS reduced significantly. The level of △ψm increased, the level of phosphorylased GSK-3β and phosphorylased PI3K protein obviously increased. The effect of CT-1 was inhibited by LY294002, but no significant effect was observed on ceils survival in DMSO group, which confirmed that LY294002 specifically in-volved blocking the protective effect of CT-1. Conclusions CT-1 can protect cardiac cells against hypoxia- reoxy-genation injury, these effects are dependent upon its ability to activate the PI3K/GSK-3β pathway.
ABSTRACT
AIM: To observe the change of subunit of NADPH oxidation enzyme complex nox - 1 protein in cardiocyte hypoxia - reoxygenation injury and the role of cardiotrophin -1.METHODS: Cardiomyocytes from the hearts of 1 -3 d old neonatal rats were prepared by a modified method. Five groups were included in the study: control; hypoxia/ reoxygenation; hypoxia/reoxygenation + CT - 1; CT - 1 + hypoxia/reoxygenation + LY294002 (PIK3/Akt inhibitor) ; CT -1 + hypoxia/reoxygenation + PD98059 (ERK inhibitor) ; CT - 1 + hypoxia/reoxygenation + DMSO. The concentration of CT -1 was 10 μg/L. The survival rate of myocytes was evaluated by MTS method. Apoptosis, mitochondrial permeability transition pore ( △ψm) and reactive oxygen species ( ROS) were detected by flow cytometry. Nox - 1 protein was determined by Western blotting. RESULTS: Apoptosis of cardiomyocytes and the level of ROS (19.7% ±1.4% vs 2.1% ± 0.5% , 14.07% ± 1.25% vs 3.54% ± 0.86% , P < 0.05 ) increased markedly after hypoxia/reoxygenation, but cardio-myocyte survival rate and the level of△ψm (40.55% ±4.25% vs 86.28% ±7.15% , P <0.01) decreased significantly. The expression of nox - 1 protein was upregulated markedly. With CT - 1 intervention, cardiomyocyte survival rate increased markedly, apoptosis, both ROS and expression of nox - 1 protein reduced significantly. The level of△ψm increased obviously. The effect of CT - 1 was inhibited by LY294002.No significant effect was observed on cells survival in DMSO group, which confirmed that LY294002 was specifically involved in blocking the protective effect of CT - 1.CONCLUSION : The expression of subunit of NADPH oxidation enzyme complex nox - 1 protein is upregulated markedly in cardiocyte hypoxia - reoxygenation injury.CT - 1 protects cardiac cells against hypoxia - reoxygenation injury by downregulating the expression of nox -1 protein to decrease the level of ROS.