ABSTRACT
Objective:To detect the effect of Celecoxib on the proliferation and apoptosis of human nasopha-ryngeal carcinoma cell line CNE-2. Method:The growth inhibition rate of CNE-2 by Celecoxib was evaluated with MTT method. Apoptosis related morphology changes were observed with transmission electron microscopy (TEM). The cell cycle and apoptosis were measured with flow cytometric method (FCM). Apoptotic index ( AI) was counted by the TDT-mediated dUTP-biotin nick end-labeling (TUNED assay. Result: The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner. Apoptosis with nuclear chromatin condensa-tion, cell shrinkage, periplast loss and the formation of apoptotic bodies was observed with TEM. Apoptotic rates of CNE-2 cells treated with 80 and 100 μmol/L celecoxib were (10. 47±0. 18)% and (20. 17±0. 55)% respective-ly, significantly higher than those of the control group (1. 57±0. 27)% with FCM. The percentage of G_0/G_1 phase cells increased, whereas the S and G_2/M phases cells decreased in a dose-dependent manner after the treatment. TUNEL assay showed that the apoptosis ratio( AI) of CNE-2 treated with Celecoxib was higher than control group (P<0. 01). Conclusion:Celecoxib can inhibit the growth of human nasopharyngeal carcinoma cell line CNE-2 and induce the cell apoptosis, which may be related to blocking the cell cycle progress of CNE-2 cells.
ABSTRACT
Objective To investigate the growth inhibition and radiosensitization of Celecoxib in hu-man nasopharyngeal carcinoma cell line CNE-2. Methods CNE-2 growth inhibition by Celecoxib was eval-uated by MTT method. Apoptosis-related changes in morphology were observed by transmission electron mi-croscopy (TEM). Cell cycle distribution and apoptosis rate were measured by flowcytometry (FCM). The ex-pression of COX-2 protein was observed by SP method after the treatment of Celecoxib. Cells were randomly planted into four groups: irradiation control(Ci), drug group(Cd), irradiation group(R), and Celecoxib plus irradiation group(D+R). Single irradiation of 2,4,6,8,and 10 Gy were administered for colonogenic assay. Cell cycle distribution and apoptosis rate were analyzed at 6 Gy irradiation. Results The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner, the IC50 was 80 μmol/L After the treatment, cell ratio of GO and G, phases was increased (47.03±2.76 vs 56.17±1.95, t=4.68, P= 0.010), whereas the ratio of S and G2/M phases was decreased (33.07±1.86 vs 24.87±1.76, t=5.54, P = 0.010; 19.30±0.53: 17.73±0.83, t=2.75, P=0.050), and the apoptosis rate was increased (1.57±0.47:10.47±0.31, t = 27.39, P = 0.000) in a dose-dependent manner. Apoptosis with nuclear chromatin condensation, fragmentation and cell shrinkage was found by TEM. SP method showed that Celeib decreased COX-2 expression (17.48±0.34 vs 12.82±0.51,t=13.20,P =0.00). The sensitivity ratio(D0) was 1.15. FCM showed that the percentage of cells in G2/M phase was significanty more in R and D+R groups than in Ci and Cd groups (68.00±1.65,54.27±5.74,17.60±0.80,14.86±1.23, t=47.70,P=0.000; t=11.63, P=0.000), and also significantly different between R group and D + R group (t=3.99, P= 0.020). The apoptosis rate was higher in R and D + R groups than Ci and Cd groups(4.83±0.97,9.50± 1.35,1.33±0.86 and 2.28±0.42,t=4.67,P=0.010;t=8.81, P=0.000), D + R group than R group(t =4.85,P=0.010). Conclusions Celecoxib can markedly inhibit the growth and induce apoptosis in CNE-2 cells,which may depend on COX-2 pathway. Celeeoxib potently enhances the radiosensitivity of CNE-2 cells,which may due to the repair inhibit of radiation-induced DNA damage, inhibit of cell proliferation,and enhancement of cell apoptosis after irradiation.
ABSTRACT
OBJECTIVE@#To detect the effect of Celecoxib on the proliferation and apoptosis of human nasopharyngeal carcinoma cell line CNE-2.@*METHOD@#The growth inhibition rate of CNE-2 by Celecoxib was evaluated with MTT method. Apoptosis related morphology changes were observed with transmission electron microscopy (TEM). The cell cycle and apoptosis were measured with flow cytometric method (FCM). Apoptotic index (AI) was counted by the TDT-mediated dUTP-biotin nick end-labeling (TUNEL) assay.@*RESULT@#The growth of CNE-2 cell was inhibited by celecoxib in a dose-and time-dependent manner. Apoptosis with nuclear chromatin condensation, cell shrinkage, periplasm loss and the formation of apoptotic bodies was observed with TEM. Apoptotic rates of CNE-2 cells treated with 80 and 100 micromol/L celecoxib were (10.47+/-0.18)% and (20.17+/-0.55)% respectively, significantly higher than those of the control group (1.57+/-0.27)% with FCM. The percentage of G0/G1 phase cells increased, whereas the S and G2/M phases cells decreased in a dose-dependent manner after the treatment. TUNEL assay showed that the apoptosis ratio (AI) of CNE-2 treated with Celecoxib was higher than control group (P<0.01).@*CONCLUSION@#Celecoxib can inhibit the growth of human nasopharyngeal carcinoma cell line CNE-2 and induce the cell apoptosis, which may be related to blocking the cell cycle progress of CNE-2 cells.
Subject(s)
Humans , Apoptosis , Celecoxib , Cell Line, Tumor , Cell Proliferation , Cyclooxygenase 2 Inhibitors , Pharmacology , Nasopharyngeal Neoplasms , Pathology , Pyrazoles , Pharmacology , Sulfonamides , PharmacologyABSTRACT
<p><b>OBJECTIVE</b>Transesophageal echocardiography was performed during closed-chest cardiopulmonary resuscitation (CPR) in in-hospital cardiac arrest to further explore the hemodynamic mechanism of CPR.</p><p><b>METHODS</b>CPR attempts were performed according to advanced cardiovascular life support guidelines in 6 cases of in-hospital cardiac arrest. Multi-plane transesophageal echocardiography was carried out within 15 min of initiation of CPR. Throughout CPR, the motion of the mitral, tricuspid and aortic valves, the changes in the left ventricular cavity size and the thoracic aortic diameter were observed. Trans-mitral and trans-aortic Doppler files of blood flow were also documented.</p><p><b>RESULTS</b>A closure of the mitral and tricuspid valves with simultaneous opening of the aortic valve occurred exclusively during chest compression, resulting in forward blood flow in the pulmonary and systemic circulation. Peak forward aortic flow at a velocity of 58.8 +/- 11.6 cm/s was recorded during the compression phase. Whereas, a closure of the aortic valve and rapid opening of the atrioventricular valves associated with ventricular filling during relaxation of chest compression was noted in all 6 patients. Peak forward mitral flow at a velocity of 60.6 +/- 20.0 cm/s was recorded during the release phase. Mitral regurgitation during the chest compression period was detected in 5 patients, reflecting a positive ventricular-to-atrial pressure gradient. A reduction in the left ventricular chamber and an increase in the thoracic aortic diameter during the compression phase was found in all patients, indicating that direct cardiac compression contributed to forward blood flow.</p><p><b>CONCLUSION</b>These observations favor the cardiac pump theory as the predominant hemodynamic mechanism of forward blood flow during CPR in human beings.</p>
Subject(s)
Aged , Aged, 80 and over , Female , Humans , Male , Middle Aged , Cardiopulmonary Resuscitation , Echocardiography, Transesophageal , Heart Arrest , Diagnostic Imaging , Therapeutics , HemodynamicsABSTRACT
Objective To observe the effect of heat stress on plasma cGMP and hemodynamics in animals with chronic heart failure. Methods Coronary arteries of twenty-five rabbits were ligated to set up the animal model of heart failure and other five rabbits only received thoractomy as sham group. Eight weeks after coronary artery ligation, they are randomly divided into heat stress (HS) group, control group, HS+L-NAME group, and non-HS+L-NAME group and non-HS+L-Arg group, each group containing 5 animals. Hemodynamic indices and plasma levels of NOS and cGMP were measured. Results Hemodynamics of all 25 rats received operation was poorer compared with the rats of sham group (P
ABSTRACT
To investigate the relationship between endothelium dysfunction and experimental vasospasm, twenty-eight New Zealand white rabbits were randomly allocated into three groups: sham operation control group(Group 1, n=8), balloon endothelial denudation + normal diet group (Group 2, n=8) and balloon endothelial denudation + hypercholesterol diet group (Group 3, n=12). Angiography was performed to detect the vasospasm induced by ergonovine and endothelium-dependent vasodilator response induced by acetylcholine before and immediately after denudation and 8 week later. Visible vasospasm was induced at the denuded sites in group 3, and endothelium dysfunction was also found in the same locations. Positive correlation was showed between vasospasm and endothelium dysfunction. Endothelium dysfunction resulted from balloon endothelial denudation and hypercholesterolemia may play an important role in the pathogenesis of experimental vasospasm.