ABSTRACT
Objective To investigate the molecular protective mechanisms of myocardial hypertrophic preconditioning by mitochondrial quantitative proteomics. Methods Fourteen C57BL6/ J male mice were randomly divided into sham group(n = 6) and cardiac hypertrophy preconditioning group(n = 8). The murine model of cardiac hypertrophy preconditioning was established by imposing transverse aortic constriction for 3 days and debanding the aorta for 4 days. Three mice from sham group and four mice from cardiac hypertrophy preconditioning group were randomly selected for proteomic analysis, and the remaining mice were used for functional and morphological experiments. The cardiac function was detected by echocardiography, and mechanical properties of cardiomyocytes were assessed using a SoftEdge Myocam. Cardiac morphology and mitochondrial ultrastructure were detected by pathological sections and transmission electron microscopy. The most significant mitochondrial proteins were screened by label-free quantitative proteomics and analyzed by bioinformatics analysis. Western blotting was used to verify the expression changes. Results Compared with the sham group, there were no significant changes in cardiac function and myocardial tissue morphology in the cardiac hypertrophy preconditioning group. However, electron microscopy analyses showed that the density of mitochondrial cristae increased in cardiac hypertrophy preconditioning group. Proteomic analysis screened 20 differentially expressed mitochondrial proteins. Bioinformatics analysis revealed that differentially expressed proteins were mainly related to mitochondrial ribosomal proteins. Western blotting results of key proteins were consistent with proteomic analysis. Conclusion Myocardial hypertrophic preconditioning can promote the energy metabolism of myocardial mitochondria, which may be related to the transcription, processing and transportation of mitochondrial oxidative phosphorylation complex mediated by mitochondrial ribosomal proteins.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate whether inhaled sevoflurane is capable of producing delayed cardioprotection effect in rats and its underlying mechanisms.</p><p><b>METHODS</b>Male Sprague-Dawley rats inhaled 1.0 minimum alveolar concentration (MAC) sevoflurane, 1.5 MAC sevoflurane,or O(2) for 1 h. After 24 h and 48 h the left coronary artery of rats was occluded for 30 min,followed by 120 min of reperfusion. Hemodynamics was continuously recorded and myocardial infarct size was determined by Evans blue and triphenyltetrazolium chloride staining. The expression of nitric oxide synthase (NOS) was assessed by immunoblotting.</p><p><b>RESULTS</b>1.0 MAC sevoflurane and 1.5 MAC sevoflurane improved cardiac pump function after reperfusion and reduced myocardial infarct size with the increased iNOS expression (P<0.05). However,the expression of eNOS and p-eNOS was not affected (P>0.05). A selective iNOS inhibitor 1400 W abolished the cardioprotection effect induced by inhalation of 1.0 MAC sevoflurane for 24 h.</p><p><b>CONCLUSION</b>Sevoflurane produces delayed cardioprotection through the up-regulation of iNOS expression.</p>
Subject(s)
Animals , Male , Rats , Anesthetics, Inhalation , Pharmacology , Disease Models, Animal , Ischemic Preconditioning, Myocardial , Methyl Ethers , Pharmacology , Myocardial Reperfusion Injury , Pathology , Myocardium , Pathology , Nitric Oxide Synthase Type II , Metabolism , Rats, Sprague-Dawley , Up-RegulationABSTRACT
<p><b>OBJECTIVE</b>To prepare tanshinone microemulsion (Tan-ME) and investigate its properities and the absorption character in rat intestine in situ.</p><p><b>METHOD</b>The microemulsions were prepared and characterized using Zetapals Zeta potential/particle size analysis and atomic force microscope. A HPLC method for determination of tanshinone IIA in the intestinal flux was established. RESUILT: The Tan-ME was fine droplet with an average droplet size of (32.25 +/- 6.59) nm. The results of Tan-ME absorption in small intestinal indicated that Tan-ME could improve the absorption of tanshinone IIA in rat small intestine, but the absorption coefficient of Tan-ME, Ka was influenced by the ratio of water-phase in Tan-ME.</p><p><b>CONCLUSION</b>Tan-ME could improve the absorption of tanshinone IIA in rat small intestine. Thus bioavailability of tanshinone was improved.</p>