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OBJECTIVE@#To explore the inhibitory effect of calcitonin gene-related peptide (CGRP) on cardiac fibroblast proliferation and collagen synthesis induced by isoprenaline and the underlying mechanism.@*METHODS@#The primary cultured cardiac fibroblasts were incubated with isoprenaline (10(-5) mol/L) for 48 h after pretreatment with CGRP (10(-8) or 10(-7) mol/L) for 1 h. Cell activity was detected by MTT. The mRNA expression of collagen (types I and III) and connective tissue growth factor (CTGF) was determined by RT-PCR, and the levels of intracellular ROS were determined by DCFH-DA fluorescent probe.@*RESULTS@#Isoprenaline significantly promoted fibroblast proliferation and up-regulated collagen (types I and III) and CTGF mRNA expression concomitantly with an increase in ROS production, which were attenuated by CGRP. The effect of CGRP on cardiac fibroblasts was inhibited by CGRP8-37, a selective antagonist of CGRP receptor.@*CONCLUSION@#CGRP is able to protect cardiac fibroblasts against isoprenaline-induced proliferation and collagen expression, which might be related to the down-regulation of CTGF expression through inhibition of ROS production.
Sujet(s)
Animaux , Rats , Animaux nouveau-nés , Peptide relié au gène de la calcitonine , Pharmacologie , Prolifération cellulaire , Cellules cultivées , Collagène de type I , Génétique , Métabolisme , Collagène de type III , Génétique , Métabolisme , Facteur de croissance du tissu conjonctif , Génétique , Métabolisme , Fibroblastes , Biologie cellulaire , Isoprénaline , Pharmacologie , Myocytes cardiaques , Biologie cellulaire , Culture de cellules primaires , ARN messager , Génétique , Métabolisme , Rat Sprague-Dawley , Espèces réactives de l'oxygène , MétabolismeRÉSUMÉ
Objective To explore the inhibitory effect of calcitonin gene-related peptide (CGRP) on cardiomyocyte apoptosis and the underlying mechanism.Methods In cultured rat cardiomyocytes,apoptosis was induced by the incubation of isoprenaline ( 10ˉ5 mol/L) for 48 h.CGRP ( 10ˉ8 or 10ˉ7 mol/L) was administrated for 1 h before incubating isoprenaline to evaluate its effect on cardiomyocyte apoptosis.At the end of the drug treatment,the rate of apoptotic cells and intracellular reactive oxygen species (ROS) were determined,and RNA was extracted to examine the expression of microRNA-1 and microRNA-133a.Results Isoprenaline significantly increased the rate of apoptotic cells and intracellular ROS production concomitantly with the increased microRNA-1 expression and the decreased microRNA-133a expression,which were inhibited by pretreatment with CGRP.The effects of CGRP were reversed by CGRP receptor antagonist.Conclusion CGRP can inhibit the isoprenaline-induced cardiomyocyte apoptosis.The beneficial effect of CGRP is related to regulating microRNA-1 and microRNA-133a expression through the prevention of isoprenaline-induced ROS production.
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0.05). Compared with the altitude of 1 507 m group, the activity of SOD and GSH-Px significantly decreased in the altitude of 3 850 m and 2 500 m groups, it was contrary in the content of MDA (P
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AIM: To investigate the effect of cold exposure on the thermoregulatory function in hypothyroid rats. METHODS: Hypothyroid model was established by administration of antithyroid drug propylthiouracil(PTU) in rats. Colonic temperature was measured using digital thermometer. Plasma T_3 and T_4 concentrations were determined by radioimmunoassay. The effect of cold exposure on body temperature was observed after 2 weeks of PTU treatment. RESULTS: Plasma T_3 and T_4 concentrations were reduced markedly 2 weeks after PTU treatment, and colonic temperature was also decreased markedly; Hyperthermic response was not different between PTU group and control group during cold exposure. CONCLUSION: This study suggests that PTU-induced hypothyroid rat possesses a robust thermogenic response to short bouts of cold exposure.
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AIM: To inverstigate the protective effects of procyanidin on myocardial ischemia reperfusion injury in rats. METHODS: Myocardial ischemia reperfusion injury models were established by the ligation of left desending coronary artery for 40 min and referfusion for 120 min in rats, and the influence of procyanidin on enzymes of myocardial, myocardial infarction size and lipid peroxide were observed. RESULTS: Procyanidin decreased myocardial creatine phosphokinase (CPK) and lactate dehydrogenase (LDH) release significantly diminished myocardial infarction size, raised the activity of superoxide dismutase (SOD), reduced malondialdehyde (MDA) content in myocardial and serum in comparison with the control. CONCLUSION: Procyanidin has a protective effect on myocardial ischemia reperfusion injury. The action is related to the inhibition of the free radical and subsequent lipid peroxidation.