ABSTRACT
To observe the effects of hypothermia on the repolarization duration and the expression of Kir2.1 protein of ventricular myocytes in isolated rat heart and explore the role of Kir2.1 protein. Eighteen healthy adult male Sprague-Dawley rats were randomly divided into three groups (n=6 per group): Control group (C group), 35℃ group (H group), 32℃ group (H group). Langendorff isolated heart models were established. After 15 min 37℃ K-H fluid banlanced perfusion, C group continued to perfuse the K-H solution at 37℃ for 30 minutes, H group continued to perfuse the K-H solution at 35℃ for 30 minutes, H group continued to perfuse the K-H solution at 32℃ for 30 minutes. At 15 min of balanced perfusion (T), and 30 min of continuous perfusion (T), the heart rate,and the MAP in the three layers of the left ventricular anterior wall were recorded, the action potential duration at 50% repolarization (MAPD), the action potential duration at 90% repolarization (MAPD) and transmural dispersion of repolarization(TDR) were calculated. At the same time, the occurrence of arrhythmia was recorded. The expression of Kir2.1 protein was measured by Western blot. The average optical density (AOD) and the distribution of Kir2.1 protein were measured by immunohistochemistry in the ventricular tissue measured by electrophysiology. Compared with T, the heart rate was decreased, MAPD and MAPD were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) in H group, H group at T. Compared with C group, the HR was decreased, the MAPD was prolonged significantly (P＜0.05), TDR was increased significantly (P＜0.05),the expression and the AOD of Kir2.1 protein were decreased significantly (P＜0.05) in Hgroup, Hgroup at T. Compared with H group, the heart rate of H group was decreased significantly (P＜0.05), MAPD and MAPD were prolonged significantly (P＜0.05), and TDR was increased significantly (P＜0.05) at T. The distribution of Kir2.1 protein in group C was normal, while the distribution of Kir2.1 in H group and H group was disordered. Hypothermia prolonged the ventricular duration of repolarization and increased the dispersion of repolarization. The mechanism is related to the down-regulation the expression of Kir2.1 protein and the disorder of the distribution of Kir2.1 protein.
ABSTRACT
Epimedium was obtained from different habitats, and their bioactive components for inhibiting RAW264.7 were screened by MTT assay. Results indicate that epimedium from different habitats displayed significant different activities. By means of model population analysis (MPA), a latent bioactive component, baohuoside-I was got. Activity of baohuoside-I wasvalidated and prior to icariin. MPA can be used for bioactive components screening.
Subject(s)
Humans , Cell Proliferation , Cytological Techniques , Methods , Drugs, Chinese Herbal , Pharmacology , Epimedium , Chemistry , Flavonoids , Pharmacology , Osteoclasts , Cell Biology , Plants, Medicinal , ChemistryABSTRACT
<p><b>OBJECTIVE</b>To determine whether smoking affects the endothelial function of young ED patients with no cardiovascular disease.</p><p><b>METHODS</b>This study included 69 ED patients (21 smokers and 48 non-smokers) and 16 age-matched normal healthy controls. All underwent measurement of brachial artery flow-mediated vasodilation (FMD) and examinations of blood pressure, cholesterol, triglycerides and glucose.</p><p><b>RESULTS</b>Brachial artery FMD was remarkably decreased in the ED patients, even more significantly in the smokers ([6.0 +/- 0.8]%) than in the non-smokers ([9.7 +/- 2.5]%) (P < 0.05), as compared with that in the normal healthy controls ([14.0 +/- 2. 5]%, P < 0.05).</p><p><b>CONCLUSION</b>Endothelial function is impaired in ED patients, and is further damaged by smoking.</p>
Subject(s)
Adult , Humans , Male , Case-Control Studies , Endothelium, Vascular , Erectile Dysfunction , Impotence, Vasculogenic , Smoking , VasodilationABSTRACT
<p><b>OBJECTIVE</b>To study the mechanisms of oridonin-induced U937 cell apoptosis, and to examine the role of ERK MAPK.</p><p><b>METHOD</b>MTT, Hoechst 33258 staining, DNA agarose gel electrophoresis and Western blot analysis were used.</p><p><b>RESULT</b>Oridonin inhibited U937 cell growth in a time- and dose-dependent manner. Apoptotic bodies were found with Hoechst 33258 staining after treatment with 27 micromol x L(-1) oridonin. Simultaneously, ERK phosphorylation was significant. ERK inhibitor PD98059 partially blocked the growth-inhibitory effect as well as DNA fragmentation. The expression of antiapoptotic mitochondrial protein Bcl-XL decreased time-dependently, and that of proapoptotic protein Bax increased. However, PD98059 reversed the effect of oridonin on Bcl-XL and Bax.</p><p><b>CONCLUSION</b>Oridonin induces U937 cell apoptosis through activation of ERK and alteration of the ratio of Bax/Bcl-XL.</p>