葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

葡萄糖酸镁对离体大鼠心肌缺血再灌注细胞凋亡的影响

Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.     

缬沙坦/氨氯地平和依贝沙坦/双氢克尿噻联合治疗老龄高血压疗效的研究

Objective To compare the clinical effect of valsartan/amlodipine combination or irbesartan/hydrochlorothiazide(HCTZ)combination in very elderly hypertensives.Methods After a 4-week placebo period,94 hypertensives,aged 75-89 years were random given valsartan 160 mg/amlodipine 5 mg or irbesartan 300 mg/HCTZ 12.5 mg for 24 weeks according to a rospective study.After 4 weeks,amlodipine or HCTZ was doubled in non-responders.Patients were checked every 4 weeks.At each visit,sitting,lying and standing blood pressure(BP),systolic BP(SBP)and diastolic BP(DBP)were measured. At the end of placebo period and treatment period,electrolytes and uric acid were evaluated.Results Blood pressure was significantly decreased in both treatment groups,however,there was no statistical significance between two groups.BP changes from lying to standing position were significantly greater in the irbosartan/HCTZ group(-17.2/-9.1 mmHg)than that in the valsartan/amlodipine group(-10.1/-1.9 mmHg,t=2.14,P＜0.05 for SBP and t=3.11,P＜0.01 for DBP vs.irbesartan/HCTZ).Potassium significantly decreased and uric acid significantly increased(-0.4 mmol/L,t = 2.33,P＜ 0.05 and+29.7μ mol/L,t =2.54,P＜0.05 vs.baseline,respectively)only in the irbesartan/HCTZ group.Conclusions Both combinations had similarly effective in reducing clinical BP in very elderly hypertensives.However,valsartan/amlodipine offered some advantage and less pronounced BP orthostatic changes and absence of metabolic adverse effects.     

罗格列酮与全反式维甲酸对人胃癌SGC7901细胞株生长和凋亡的影响

Objective To investigate the influence of PPARγ excitomotor RSG and ATRA on gastric cancer SGC7901 cell line proliferation in vitro and its potential mechanism study.Methods Human gastric cancer SGC7901 cell line was cultured in vitro.Experiment samples were divided to blank group,10μmol/L ATRA group, 12.5μmol/L RSG group, 25μmol/L RSG group, 10μmol/L ATRA + 25μmol/L RSG group.Proliferation inhibitory effect was determined by MTI assay.Flow cytometry was used to detect cell cycle, H.E stain was used to observed micrography alteration.Expression of PPARγ protein in gastric cancer cells were measured by immunohistochemistry.PPARγ mRNA in gastric cancer cells were measured by RT-PCR.Results ATAR at concentration 10μmol/L, RSG at 12.5 μmol/L and RSG at 25 μmol/L could inhibit the proliferation of SGC7901 cells in a dose-and time-dependent, and when both agents were combined for 72h, growth inhibition ratio was (29.73 ± 0.69) %.Flow cytometry analysis revealed a cell cycle arrest at G1 and S phase, and when both agents combined, S% was (12.87 ± 0.35 )%, cell micrography tended to be normal when both agents combined.Up-regulation of PPARγ protein and PPARγ mRNA expressions were also observed, those effects were enhanced when both agents combined, and grey scale ratio was 0.646.Conclusion The ATRA and RSG could significantly induced growth inhibition of human gastric cancer SGC7901 cell, which may be associated with cell cycle arrest and inducing differentiation, activation of PPARγ protein and PPARγ mRNA expression.Synergistic effect could be caused by the combined use of the two agents.     

罗格列酮与全反式维甲酸对人胃癌SGC7901细胞株生长和凋亡的影响

Objective To investigate the influence of PPARγ excitomotor RSG and ATRA on gastric cancer SGC7901 cell line proliferation in vitro and its potential mechanism study.Methods Human gastric cancer SGC7901 cell line was cultured in vitro.Experiment samples were divided to blank group,10μmol/L ATRA group, 12.5μmol/L RSG group, 25μmol/L RSG group, 10μmol/L ATRA + 25μmol/L RSG group.Proliferation inhibitory effect was determined by MTI assay.Flow cytometry was used to detect cell cycle, H.E stain was used to observed micrography alteration.Expression of PPARγ protein in gastric cancer cells were measured by immunohistochemistry.PPARγ mRNA in gastric cancer cells were measured by RT-PCR.Results ATAR at concentration 10μmol/L, RSG at 12.5 μmol/L and RSG at 25 μmol/L could inhibit the proliferation of SGC7901 cells in a dose-and time-dependent, and when both agents were combined for 72h, growth inhibition ratio was (29.73 ± 0.69) %.Flow cytometry analysis revealed a cell cycle arrest at G1 and S phase, and when both agents combined, S% was (12.87 ± 0.35 )%, cell micrography tended to be normal when both agents combined.Up-regulation of PPARγ protein and PPARγ mRNA expressions were also observed, those effects were enhanced when both agents combined, and grey scale ratio was 0.646.Conclusion The ATRA and RSG could significantly induced growth inhibition of human gastric cancer SGC7901 cell, which may be associated with cell cycle arrest and inducing differentiation, activation of PPARγ protein and PPARγ mRNA expression.Synergistic effect could be caused by the combined use of the two agents.     

硝酸甘油对大鼠重症急性胰腺炎ET/NO、TXA2/PGI2的影响

Objective To explore the effect of nitroglycerin on ET/NO, TXA2/PGI2 and pancreas pathomorphology changes in severe acute pancreatitis (SAP) rats. Methods Sixty SD rats were random divided into five groups, including control group (A group, n = 12) and experimental group(B,C,D and E group, n = 12). The SAP was induced by injection of 5% sodium taurocholate through retrograde common biliopancreatic ducts via duodenal papilla with epidural catheter. Group C, D and E were intravenously injected with nitroglycerin 0.5μg/kg/min,1μg/kg/min and 2μg/min in 30 min respectively, and group A and B was injected with Sodium Chloride 0.5ml. The indexes of changed pathomorphology and ET/NO, TXB2/6-keto-PGF1a, were determined at the 6th and 12th hour after operations, respectively. Results The specimen data of the 6th and 12th hour displayed that the indexes of changed pathomorphology, ET, ET/NO, TXB2, and TXB2/6-keto-PGF1a of the group C,D and E degraded respectively, compared to group B(P < 0.05). Conclusion The nitroglycerin could degrade ET, ET/NO,TXA2 and TXA2/PGI2, improve the microcirculation of pancreas, and delay the pathological inflammation change in SAP rats.     

利尿剂在三聚氰胺及三聚氰酸致大鼠急性肾损伤中的治疗作用

Objective To investigate the effect of diuretic (furosemide) therapy on kidney injury induced by melamine and cyanuric acid in rats. Methods 36 male Spragne Dawley rats were random disided into 3 groups. Group A was treated with 2mL of water daily, group B was treated with melamine and cyanuric acid ( each 100 mg/kg) daily for 4 days and then 2ml of water daily, group C was treated with the same as group B at the first 4 days and then treatment with furosemide (20mg/kg) daily. Samples of blood and 24h urine were collected to detective biochemical indexes, and kidney sections were performed on days 4 and 11 ( each end point, n = 6). The kidneys were observed with histopathology and renal crystal deposition scores were determined. Results On the 4th day, group B and group C were resulted in acute kidney injury such as oliguria [ ( 3. 39 ± 1.02 ) ml, ( 3. 20 ± 0. 86 ) ml ] and high serum creatinine [ ( 153.54 ±27. 08)μmol/L, (160. 11 ± 19. 55)μmol/L] and renal melamine cyanurate crystal were found in the renal tissues. On the 11th day, the renal crystal deposition score in the rats was reduced by 9. 52% ( P >0. 05). Compared with those of the 4th day in group B, it reduced by 63.63%( P <0.05) in group C. Urine volume were increased significantly compared with those of the 4th day( P < 0. 05 ) in group C [ from (3.20±0. 86)ml to (25.96 ±5.97)ml] and group B [ from(3. 39 ± 1.02)ml to (8. 57 ± 1.66)ml] , and Urine volume in group C was increased significantly more than that in group B ( P < 0. 05 ). The serum creatinine was obviously reduced as compared with those of the 4th day in group B and C( P <0.05), from[ (153. 54±27.08) μmol/L] to [ ( 106. 10 ±5.53) μmol/L] in group B and from [ ( 160. 11 ± 19. 55) μmol/L] to [ (67. 17 ± 12. 80 ) μmol/L] in group C, but the serum creatinine in group B was still higher than that in group A and C ( P < 0. 05). Conclusions Furosemide can attenuate the damage of acute kidney injury induced by melamine and cyanuric acid.     

近视眼视网膜神经纤维层厚度与中央角膜厚度相关性研究

Objective To explore the relationship between retinal nerve fiber layer (RNFL) thickness and central corneal thickness (CCT) in myopia eyes.Methods 91 cases (91eyes) were selected from ophthalmological outpatients including 28cases with low myopia ( spherical equivalence [ SE ] ＞ -3.0D), 33 cases with moderate myopia (SE -0.3D ～ -6.0D) and 30 cases with high myopia (SE ＜ -6.0D).All patients received ocular standard examination including intraocular pressure, refraction, slitlamp biomicroscopy and fundus examination.Other ocular diseases except refractive error were excluded.RNFL thickness and CCT were measured by RTVue Fourior-OCT ( Optovue Inc, USA).Refraction diopter was shown as SE.Results The mean RNFL thickness and CCT was ( 108.5 ± 10.1 ) μm, (524.7 ±36.8)μm respectively.These were no significantly different among low, moderate and high myopia ( P ＞ 0.05 ).Temporal RNFL thickness( tl1 ,tu1 ) was significantly positive related with CCT( r =0.281,0.093 of tl1, r= 0.352,0.167 of tu1 respectively in single and multiple variable analysis; P ＜ 0.05 ), nasal ( nl2, nu2)and inferior nasal RNFL thickness( in2,in1 )was significantly positive related with SE( P ＜0.05), inferior temporal RNFL thickness( it2)was significantly negative related with SE( P ＜0.05), and RNFL thickness in other regions were not significant related with CCT and SE ( P ＞ 0.05 ) in single and multiple variable regressive analysis.Conclusion Relationship between RNFL thickness of local paradisc region and CCT in myopia eyes suggested that CCT should be correlative with some sensible structural parameters in glaucomatous neuropathy and might be important in the diagnosis and therapy of glaucoma.     

近视眼视网膜神经纤维层厚度与中央角膜厚度相关性研究

Objective To explore the relationship between retinal nerve fiber layer (RNFL) thickness and central corneal thickness (CCT) in myopia eyes.Methods 91 cases (91eyes) were selected from ophthalmological outpatients including 28cases with low myopia ( spherical equivalence [ SE ] ＞ -3.0D), 33 cases with moderate myopia (SE -0.3D ～ -6.0D) and 30 cases with high myopia (SE ＜ -6.0D).All patients received ocular standard examination including intraocular pressure, refraction, slitlamp biomicroscopy and fundus examination.Other ocular diseases except refractive error were excluded.RNFL thickness and CCT were measured by RTVue Fourior-OCT ( Optovue Inc, USA).Refraction diopter was shown as SE.Results The mean RNFL thickness and CCT was ( 108.5 ± 10.1 ) μm, (524.7 ±36.8)μm respectively.These were no significantly different among low, moderate and high myopia ( P ＞ 0.05 ).Temporal RNFL thickness( tl1 ,tu1 ) was significantly positive related with CCT( r =0.281,0.093 of tl1, r= 0.352,0.167 of tu1 respectively in single and multiple variable analysis; P ＜ 0.05 ), nasal ( nl2, nu2)and inferior nasal RNFL thickness( in2,in1 )was significantly positive related with SE( P ＜0.05), inferior temporal RNFL thickness( it2)was significantly negative related with SE( P ＜0.05), and RNFL thickness in other regions were not significant related with CCT and SE ( P ＞ 0.05 ) in single and multiple variable regressive analysis.Conclusion Relationship between RNFL thickness of local paradisc region and CCT in myopia eyes suggested that CCT should be correlative with some sensible structural parameters in glaucomatous neuropathy and might be important in the diagnosis and therapy of glaucoma.     

降钙素对大白兔糖尿病骨质疏松模型假体骨密度及生物力学的影响

Objective To investigate the influence of calcitonin on bone mineral density and biomechanics around the artificial pros-thesis in ovariectomized diabetic rabbit model. Methods Fourteen femina New Zealand white rabbits at the age of 5 months old were select-ed, which weight 2.24 -2.65kg, averaging 2.26kg. First, the model of rabbit with diabetic osteoporosis was successfully established by the compound method of ovariectomy plus streptozotocin. Osteotomy in the middle part of femur was performed in both groups, fixation of artifi-cial prosthesis was done with 3.0 kirschner wire. After that, Rabbit models with diabetic osteoporosis were randomly divided into experimen-tal group and control group. Rabbits in the experimental group were treated with calcitonin 6U intramuscular injection once every other day. In control group, intramuscular injection of normal saline solution 1.5ml once every three days. Rabbit models of two groups were sacrificed in the 24th week. The BMD of the region of interest (ROI) around the prosthesis were detected before experiment and 8, 16 and 24 weeks after injection. After rabbits were killed, experimental femurs in both groups were complete removal and soft tissues were rejected. Determi-nation of the pull-out and torsion bone biomechanics experiments of prosthesis was done in both groups respectively. Results The BMD of ROI in the experimental group before operation was (0.1863±0.004)g/cm2 and (0.1753±0.005)g/cm2 in 24 weeks after operation, in control group before operation was (0.1865±0.002)g/cm2 and (0.1638±0.005)g/cm2 in 24 weeks after operation. There were significant difference between the two groups(P < 0.05). Biomechanical show that the pull-out strength in the experimental group was (312.68±8.73 )N/cm2 and (205.43±12.45 ) N/cm2 in control group. There were significant difference between the two groups(P < 0.05). The tor-sion strength in experimental group was (80.47±2.51) N/cm2 and (38.52±0.64) N/cm2 in control group. There were significant differ-ence between the two groups(P < 0.05). Conclusion Salmon calcitonin can reduce the bone turnover rate around prosthesis and decrease bone absorption in the rabbit of diabetic osteoporosis models, accelerate the bone formation around prosthesis, and increase the BMD. It can ameliorate the quality of bone around prosthesis, improve its biomechanics property, and increase the holding power between prosthesis and body mass. It is of clinical significance for the prevention and treatment of aseptic loosening artificial prosthesis.     

关节腔内注射洛伐他汀预防骨关节炎软骨退变

目的 研究洛伐他汀关节腔内注射对骨关节炎(OA)模型关节软骨退变及对基质金属蛋白酶(matrix metalloprotein-ase-1,3)mRNA表达的影响.方法 30只6个月龄新西兰大白兔行右膝关节前交叉韧带切断术.手术后将动物随机分为实验组和对照组,实验组术后立即给予关节腔内注射0.5 mg/ml洛伐他汀0.2 ml/kg,每周1次,连续6周;对照组则关节腔内注射等容量的生理盐水.术后6周处死动物.在解剖镜下观察股骨内髁关节软骨的大体形态学改变并评分.用反转录-聚合酶链式反应检测软骨及滑膜中MMP-1,3 mRNA的表达.结果 解剖镜下实验组软骨退变程度较对照组明显减轻;实验组关节液中IL-1水平较对照组明显降低;实验组滑膜中MMP-1,3 mRNA的表达水平显著低于对照组(P<0.05),而软骨中的MMP-1,3 mRNA的表达较对照组差异无统计学意义(P>0.05).结论 在OA早期关节腔内注射L洛伐他汀能够明显降低MMP-1,3 mRNA的表达,减轻骨关节炎软骨的退变.     

血清基质金属蛋白酶3与颈动脉粥样硬化斑块及缺血性脑卒中的关系

Objective To investigate the relationship between the matrix metalloproteinase-3(MMP-3)and the stability of carotid artery plaque,and explore MMP-3's prediction role on the attack and relapse of acute ischemic cerebrovascular events.Methods 100 patients with the first ever acute cerebral infarction,100 patients with chronic cerebral circulation insufficiency(CCCI)and 40 persons without cerebrovascular diseases were enrolled in this study.According to the carotid ultrasound examination,100 cerebral infarction patients were divided into three subgroup: unstable plaque group(45 patients,mixed plaque,soft plaque),stable plaque group(35 patients,plaque Group)and endometrial coarse group(25patients).Matrix metalloproteinase-3(MMP-3)levels of all the subjects were measured by enzyme-linked immunosorbent assay(as basal level).All the subjects were followed up for one year to observe cerebral infarction events.Serum MMP-3 levels of each group,and the basic serum MMP-3 levels were compared among patients who were attacked or relapsed cerebral ischemic with those who had not been attack cerebral ischemic during this period of time.Results 5 patients in the cerebral infarction group had relapse (5%),2 patients in the CCCI group were attacked by cerebral ischemic(2%),and no one in the normal control group was attacked by cerebral ischemic.Serum MMP-3 levels in the acute cerebral infarction group were significantly higher than CCCI group,and both groups were significantly higher than normal control group (P ＜0.05).The basic serum MMP-3 levels in all patients who were attacked by cerebral ischemic were significantly higher than those who had not been attack by cerebral ischemic during this period of time(P ＜0.05).The serum MMP-3 levels of the unstable plaque group were significantly higher than stable plaque group.And both groups were significantly higher than endometrial coarse group(P ＜0.05).Conclusions Elevated levels of matrix metalloproteinase-3(MMP-3)might have something with the stability of carotid atherosclerotic plaque,and participate the attack and the relapse of acute cerebral infarction.Determination of MMP-3 might be used to predict the attack and relapse of acute cerebral infarction.