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Objective To establish blood purification system for rats and provide a safe and reliable experimental platform for further research of blood purification. Methods The right carotid artery and the contralateral jugular vein of adult male Sprague?Dawley rats were cannulated to creat vascular access for blood purification, by which continuous arteriovenous hemofiltration blood purification system was established. Blood flow, substitution fluid flow and ultrafiltration rate were regulated by rotary mini?pumps. Blood purification therapy continued for 4 hours on the basis of maintained anesthesia and effective anticoagulation. The safety of continuous arteriovenous hemofiltration blood purification systems was evaluated by comparing the arterial blood gas, electrolyte indexes and blood glucose during the blood purification therapy. Closely monitoring the vital signs of rats, such as blood pressure and heart rate, and observing whether there were any side effects, such as massive haemorrhage, thrombogenesis and gas embolism in the therapeutic process. Results There were no obvious changes of arterial blood gas, electrolyte indexes and blood glucose during the blood purification therapy (P>0.05). The vital signs did not fluctuate acutely before and after the blood purification therapy (P>0.05). The incidence rate of side effects was very low. Conclusions Continuous arteriovenous hemofiltration blood purification system had no obvious adverse effects on healthy rats. Our blood purification system for rats appears to be safe and reliable.
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OBJECTIVE@#To investigate the role of miR-519 in regulating the cell activity of gastric cancer. @*METHODS@#The expression of miR-519 was measured by qPCR. The protein expression of HuR was detected by Western blot. MTT assay was used to detect the cell activity of gastric cancer cells. @*RESULTS@#The protein level of HuR in the gastric cancer cells was higher than that in the control cells. Over-expression of HuR resulted in the increase in the cell activity of gastric cancer (P<0.001). Suppression of HuR decreased the cell activity of gastric cancer (P=0.001). The miR-519 level in the gastric cancer cells was lower than that in the control cells (P=0.001). Over-expression of miR-519 decreased the protein level of HuR and the activity of gastric cancer cells. @*CONCLUSION@#MiR-may inhibit the gastric cancer cell activity through suppression of HuR expression.
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Humanos , Línea Celular Tumoral , Proliferación Celular , Proteína 1 Similar a ELAV , Genética , Metabolismo , Regulación Neoplásica de la Expresión Génica , MicroARNs , Genética , Metabolismo , Neoplasias Gástricas , Genética , MetabolismoRESUMEN
<p><b>BACKGROUND</b>Phosphatase and tensin homologue on chromosome ten (PTEN) acts as a convergent nodal signalling point for cardiomyocyte hypertrophy, growth and survival. However, the role of PTEN in cardiac conditions such as right ventricular hypertrophy caused by chronic hypoxic pulmonary, hypertension remains unclear. This study preliminarily discussed the role of PTEN in the cardiac response to increased pulmonary vascular resistance using the hypoxia-induced PH rats.</p><p><b>METHODS</b>Male Sprague Dawley rats were exposed to 10% oxygen for 1, 3, 7, 14 or 21 days to induce hypertension and right ventricular hypertrophy. Right ventricular systolic pressure was measured via catheterization. Hypertrophy index was calculated as the ratio of right ventricular mass to left ventricle plus septum mass. Tissue morphology and fibrosis were measured using hematoxylin, eosin and picrosirius red staining. The expression and phosphorylation levels of PTEN in ventricles were determined by real time PCR and Western blotting.</p><p><b>RESULTS</b>Hypoxic exposure of rats resulted in pathological hypertrophy, interstitial fibrosis and remodelling of the right ventricle. The phosphorylation of PTEN increased significantly in the hypertrophic right ventricle compared to the normoxic control group. There were no changes in protein expression in either ventricle.</p><p><b>CONCLUSION</b>Hypoxia induced pulmonary hypertension developed pathological right ventricular hypertrophy and remodelling probably related to an increased phosphorylation of PTEN.</p>
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Animales , Masculino , Ratas , Hipertensión Pulmonar , Metabolismo , Hipertrofia Ventricular Derecha , Metabolismo , Hipoxia , Metabolismo , Fosfohidrolasa PTEN , Metabolismo , Fosforilación , Ratas Sprague-DawleyRESUMEN
MicroRNA (miRNA for short) can induce mRNA cleavage or inhibit mRNA translation and regulate gene expression in the post-transcriptional level, which involves cell development, proliferation, differentiation, apoptosis, and a series of important biological processes. Recent studies have found that the abnormal regulation of miRNA's target genes may be involved in tumor resistance. And it is expected to become important tumor resistance-associat-ed molecular markers and therapeutic targets. Mechanism of traditional Chinese medicine (TCM) and its active ingre-dients can affect miRNA to regulate target proteins and target genes mediated tumor multidrug resistance. It can pro-vide new ideas for the mechanism of reversing multidrug resistance by TCM.
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AIM:To investigate the effect and mechanism of liver ischemia/reperfusion(I/R)injury on the changes of cardiac energy metabolism and structure.METHODS:48 healthy Wistar male rats were randomly divided into 6 groups as follows(n=8 in each group):control group(CTL),simply ischemia for 30 min without reperfusion(I group);reperfusion following ischemia for 30 min(I/R group);2 h reperfusion following ischemia for 30 min(I/R 2 h group);4 h reperfusion following ischemia for 30 min(I/R 4 h group)and 6 h reperfusion following ischemia for 30 min(I/R 6 h group).The level of serum endotoxin was measured.The levels of insulin and insulin antibody in heart were detected by radioimmunoassay.The contents of MDA,MPO and lactic acid in heart were also determined.RESULTS:During the process of liver I/R injury,the level of endotoxin increased in I group and I/R group and declined gradually for long time during reperfusion,but was still longer than that in CTL group(P0.05).CONCLUSION:During the process of liver I/R injury,endotoxin is absorbed from intestine and impairment of liver detoxication leads to endotoxemia,which might play a role in the changes of the energy metabolism and structure in heart.