ABSTRACT
<p><b>OBJECTIVE</b>To observe the dynamic expression of calcium-sensing receptor(CaSR) in myocardium of diabetic rats.</p><p><b>METHODS</b>Thirty male Wistar rats were randomly divided into 3 groups including control, diabetic-4 week and diabetic-8 week groups(n = 10). The type 2 diabetes mellitus models were established by intraperitoneal injection of streptozotocin (STZ, 30 mg/kg) after high-fat and high-sugar diet for one month. The cardiac morphology was observed by electron microscope. Western blot analyzed the expression of CaSR, phospholamban (PLN), a calcium handling regulator, and Ca+-ATPase(SERCA) in cardiac tissues.</p><p><b>RESULTS</b>Compared with control group, the expressions of CaSR and SERCA were decreased, while the expression of PLN was significantly increased in a time-dependent manner in diabetic groups. Meanwhile diabetic rats displayed abnormal cardiac structure.</p><p><b>CONCLUSION</b>These results indicate that the CaSR expression of myocardium is reduced in the progression of DCM, and its potential mechanism may be related to the imnaired intracellular calcium homeostasis.</p>
Subject(s)
Animals , Male , Rats , Calcium-Binding Proteins , Metabolism , Diabetes Mellitus, Experimental , Diabetes Mellitus, Type 2 , Diabetic Cardiomyopathies , Metabolism , Disease Progression , Heart , Myocardium , Metabolism , Pathology , Rats, Wistar , Receptors, Calcium-Sensing , Metabolism , Sarcoplasmic Reticulum Calcium-Transporting ATPases , Metabolism , StreptozocinABSTRACT
<p><b>OBJECTIVE</b>To observe the effect of dopamine receptor (DR2) activation on hypoxia/reperfusion injury (HRI) in the neonatal rat cardiomyocytes, and to explore its mechanism.</p><p><b>METHODS</b>The hypoxia/reperfusion (H/R) injury model was established in primarily cultured neonatal rat cardiomyocytes, and randomly assigned: control, H/R, bromocriptine (Bro) and haloperidol (Hal) groups. The cell apoptosis was detected using inverted microscope, transmission electron microscope and flow cytometry (FCM). The lactate dehydrogenase(LDH) and superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in cell medium were analyzed. The expression of mRNA and protein of caspase-3, caspase-8, caspase-9, Fas, Fas-L, Cyt C and Bcl-2 were detected by RT-PCR and Western blot, respectively.</p><p><b>RESULTS</b>Compared with the control group, apoptosis rate, LDH activity, MDA content and the expression of pro-apoptotic factors and anti-apoptotic factors were increased, but SOD activity was decreased in H/R group. Compared with the H/R group, all index above-mentioned were down-regulated or reversed in Bro-group, and had no obvious differences in Hal-group.</p><p><b>CONCLUSION</b>The neonatal rat cardiomyocytes injury and apoptosis caused by hypoxia/reperfusion can be inhibited with DR2 activation, which mechanism is related to scavenging oxygen radical.</p>
Subject(s)
Animals , Rats , Animals, Newborn , Apoptosis , Cell Hypoxia , Myocardial Reperfusion Injury , Metabolism , Myocytes, Cardiac , Cell Biology , Metabolism , Oxidative Stress , Rats, Wistar , Receptors, Dopamine D2 , MetabolismABSTRACT
OBJECTIVE@#To investigate the expression of heme oxygenase-1 (HO-1) at different intervals and to provide evidence for estimation on injury intervals after brain contusion in human.@*METHODS@#Twenty-four patients died of serious brain injury were assigned as injury group and 4 patients died of non-brain injury were served as control group. HO-1 expression was analyzed in brain tissue at different time intervals (3 h, 6-9 h, 12-24 h, 36 h-3d, 5-8d, 17-20d) by immunohistochemistry and auto-image analysis system.@*RESULTS@#The level of HO-1 expression started to increase in 3 h after brain contusion compared to the control group (P < 0.05). The level of HO-1 expression highest level in 12-24 h group, and maintained high level in 36 h-3 d, then decreased gradually.@*CONCLUSION@#The expression of HO-1 might be a strong evidence for human brain contusion time estimation.