Objective： To learn the effect of allitridi on inducing mitotic arrest in human gastric cell line SGC-7901 and its possible mechanisms. Methods： We treated SGC-7901 cells with allitridi, and observed the proliferati...Objective： To learn the effect of allitridi on inducing mitotic arrest in human gastric cell line SGC-7901 and its possible mechanisms. Methods： We treated SGC-7901 cells with allitridi, and observed the proliferation inhibitory rate with MTT colometric assay, changes of cell cycle using flow cytometry and Switzerland-Giemsa＇s staining, and morphologic changes of the microtubule structure and location changes of cyclin BI expression using immunofluorescence and confocal laser scanning microscope. Furthermore, the expression of cyclin B1 was analyzed quantitatively using Leica confocal software. Results： SGC-7901 cells were inhibited after exposure to allitridi and the IC50 was 7.2μg/ml for 24 h, 20μg/ml for 72 h. When the cells were treated with allitridi at concentrations of 3, 6, and 9μg/ml for 24 h respectively, there was a declining tendency in the percentage of G0/G1 cell but an increasing tendency in GE/M cell in the allitridi treated group compared with that of control （P〈0.01）. When cells were treated allitridi at concentration of 6 μg/ml for 24 h, its mitotic index was much higher （P〈0.01） than that of control, suggesting that allitridi caused arrest of gastric cancer cells in M phase. The cells were treated with allitridi became more shrunken and nepheloid, in which the microtubule networks disappeared, while the control cell exhibited an intact microtubule network. Contrasting with normal existence mainly in the cytoplasm, the cyclin B1 was expressed more significantly and concentrated in the nucleus after exposure to allitridi. Fluorescence intensity of cyclin B 1 protein in cells treated with allitridi was much more higher than that of control （P〈0.001）. Conclusion： Allitridican induce arrest of SGC-7901 cells in M phase, probably through enhancing microtubule depolymerization by elevating the expression of cyclin B1.展开更多
AIM: To determine the effect of allitridi on cell cycle of human gastric cancer (HGC) cell lines MGC803 and SGC7901 and its possible mechanism.METHODS: Trypan blue dye exclusion was used to evaluate the proliferation,...AIM: To determine the effect of allitridi on cell cycle of human gastric cancer (HGC) cell lines MGC803 and SGC7901 and its possible mechanism.METHODS: Trypan blue dye exclusion was used to evaluate the proliferation, inhibition of cells and damages of these cells were detected with electron microscope.Flow cytometry and cell mitotic index were used to analyze the change of cell cycle, immunohistochemistry, and RT-PCR was used to examine expression of the p21WAF1 gene.RESULTS: MGC803 cell growth was inhibited by allitridi with 24 h IC50 being 6.4 μg/mL. SGC7901 cell growth was also inhibited by allitridi with 24 h IC50 being 7.3 μg/mL.After being treated with allitridi at the concentration of 12 μg/mL for 24 h, cells were found to have direct cytotoxic effects, including broken cellular membrane, swollen and vesiculated mitochondria and rough endoplasmic reticula,and mass lipid droplet. When cells were treated with allitridi at the concentration of 3, 6, and 9 μg/mL for 24 h, the percentage of G0/G1 phase cells was decreased and that of G2/M phase cells was significantly increased (P = 0.002)compared with those in the group. When cells were treated with allitridi at the concentration of 6 μg/mL, cell mitotic index was much higher (P = 0.003) than that of control group, indicating that allitridi could cause gastric cancer cell arrest in M phase. Besides, the expression levels of p21WAF1 gene of MGC803 cells and p21WAF1 gene of SGC7901 cells were remarkably upregulated after treatment.CONCLUSION: Allitridi can cause gastric cancer cell arrest in M phase, and this may be one of the mechanisms for inhibiting cell proliferation. Effect of allitridi on cells in M phas e may be associated with the upregulation of p21WAF1 genes. This study provides experimental data for clinical use of allitridi in the treatment of gastric carcinoma.展开更多
Objective: To prove the effect of Allitridi in treating acute cerebral infarction. Methods: Millipore membrane filtering technique was adopted to systematically observe the blood rheology and the peripheralleucocytes ...Objective: To prove the effect of Allitridi in treating acute cerebral infarction. Methods: Millipore membrane filtering technique was adopted to systematically observe the blood rheology and the peripheralleucocytes filtering index of 53 healthy subjects and that of 33 patients before and after treatments, who sufferedfrom acute cerebral infarction and were confirmatorily diagnosed through CT. Results: The filtering index of peripheral leucocytes during the acute period of cerebral infarction rose significantly (6. 1397±4. 4602), and thedifference was significant compared with that of the healthy subjects (0. 8651±0. 4603, P＜0. 01 ). Treatedwith Allitridi, the patients' symptoms got improved and at the same time the filtering index of leucocytes lowered markedly(1. 6261±1. 3472). The conditions of the patients before and after treatments were obviously different(p＜0. 01). The index of the whole blood rheology was improved significantly. Conclusions: Allitridicould effectively improve the leucocytes deformation and the whole blood rheology as well, and alleviate clinicalsymptoms.展开更多
Background Allitridi is an active compound that is extracted from the garlic. It has effects of anti-atherosclerosis, anti-arrhythmias and lowering blood pressure. But the controversy about the effect on cardiac contr...Background Allitridi is an active compound that is extracted from the garlic. It has effects of anti-atherosclerosis, anti-arrhythmias and lowering blood pressure. But the controversy about the effect on cardiac contractility still exists. Methods Whole-cell patch clamp recording technique was used to record ICa,Lin single cell isolated rat ventricular myocytes. The nifedipine- sensitive L-type calcium current was recorded in the rat ventricular myocytes. Results Allitridi decreased the calcium channel current in a dose-dependent and voltage-dependent manner in ventricular myocytes of rats. The current-voltage curve was shifted upwards, on which active potential,peak potential and reverse potential showed no significant changes. The inactivation curve was shifted to more negative potential, but the activation curve and recovery curve were not altered. Allitridi had no effect on frequent-dependency of calcium current. Conclusion These results show that allitridi could concentration-dependently decrease calcium channel current in ventricular myocytes of rats.展开更多
To exploring the effect of Allitridi on anti arrhythmia, cardiac electrophysiological characteristic are detected in guinea pig atrium muscles by intracellular microelectrode technique. Result:The automaticity which a...To exploring the effect of Allitridi on anti arrhythmia, cardiac electrophysiological characteristic are detected in guinea pig atrium muscles by intracellular microelectrode technique. Result:The automaticity which adrenalin induces is inhibited at 125 and 625 umol/L. The force of contraction is weakened; the intensity time curve which reflects excitability move towards right after 625 umol/L administration. under 25、125、625 μmol/L, functional refractory period、action potential duration of 50% and 90% repolarization、 sinus cycle longness are extended, a relationship between dose and effect exist at SCL. Conclusion: Automaticity、 excitability and refractoriness not only are inhibited but also action potential durations are extended after Allitridi administration.展开更多
基金the National 10th Five-year Plan Key Technologies R & D Program of China(No.2004BA703B04-02)
文摘Objective： To learn the effect of allitridi on inducing mitotic arrest in human gastric cell line SGC-7901 and its possible mechanisms. Methods： We treated SGC-7901 cells with allitridi, and observed the proliferation inhibitory rate with MTT colometric assay, changes of cell cycle using flow cytometry and Switzerland-Giemsa＇s staining, and morphologic changes of the microtubule structure and location changes of cyclin BI expression using immunofluorescence and confocal laser scanning microscope. Furthermore, the expression of cyclin B1 was analyzed quantitatively using Leica confocal software. Results： SGC-7901 cells were inhibited after exposure to allitridi and the IC50 was 7.2μg/ml for 24 h, 20μg/ml for 72 h. When the cells were treated with allitridi at concentrations of 3, 6, and 9μg/ml for 24 h respectively, there was a declining tendency in the percentage of G0/G1 cell but an increasing tendency in GE/M cell in the allitridi treated group compared with that of control （P〈0.01）. When cells were treated allitridi at concentration of 6 μg/ml for 24 h, its mitotic index was much higher （P〈0.01） than that of control, suggesting that allitridi caused arrest of gastric cancer cells in M phase. The cells were treated with allitridi became more shrunken and nepheloid, in which the microtubule networks disappeared, while the control cell exhibited an intact microtubule network. Contrasting with normal existence mainly in the cytoplasm, the cyclin B1 was expressed more significantly and concentrated in the nucleus after exposure to allitridi. Fluorescence intensity of cyclin B 1 protein in cells treated with allitridi was much more higher than that of control （P〈0.001）. Conclusion： Allitridican induce arrest of SGC-7901 cells in M phase, probably through enhancing microtubule depolymerization by elevating the expression of cyclin B1.
基金Supported by the China State Key Basic Research Program, No. G1998051203
文摘AIM: To determine the effect of allitridi on cell cycle of human gastric cancer (HGC) cell lines MGC803 and SGC7901 and its possible mechanism.METHODS: Trypan blue dye exclusion was used to evaluate the proliferation, inhibition of cells and damages of these cells were detected with electron microscope.Flow cytometry and cell mitotic index were used to analyze the change of cell cycle, immunohistochemistry, and RT-PCR was used to examine expression of the p21WAF1 gene.RESULTS: MGC803 cell growth was inhibited by allitridi with 24 h IC50 being 6.4 μg/mL. SGC7901 cell growth was also inhibited by allitridi with 24 h IC50 being 7.3 μg/mL.After being treated with allitridi at the concentration of 12 μg/mL for 24 h, cells were found to have direct cytotoxic effects, including broken cellular membrane, swollen and vesiculated mitochondria and rough endoplasmic reticula,and mass lipid droplet. When cells were treated with allitridi at the concentration of 3, 6, and 9 μg/mL for 24 h, the percentage of G0/G1 phase cells was decreased and that of G2/M phase cells was significantly increased (P = 0.002)compared with those in the group. When cells were treated with allitridi at the concentration of 6 μg/mL, cell mitotic index was much higher (P = 0.003) than that of control group, indicating that allitridi could cause gastric cancer cell arrest in M phase. Besides, the expression levels of p21WAF1 gene of MGC803 cells and p21WAF1 gene of SGC7901 cells were remarkably upregulated after treatment.CONCLUSION: Allitridi can cause gastric cancer cell arrest in M phase, and this may be one of the mechanisms for inhibiting cell proliferation. Effect of allitridi on cells in M phas e may be associated with the upregulation of p21WAF1 genes. This study provides experimental data for clinical use of allitridi in the treatment of gastric carcinoma.
文摘Objective: To prove the effect of Allitridi in treating acute cerebral infarction. Methods: Millipore membrane filtering technique was adopted to systematically observe the blood rheology and the peripheralleucocytes filtering index of 53 healthy subjects and that of 33 patients before and after treatments, who sufferedfrom acute cerebral infarction and were confirmatorily diagnosed through CT. Results: The filtering index of peripheral leucocytes during the acute period of cerebral infarction rose significantly (6. 1397±4. 4602), and thedifference was significant compared with that of the healthy subjects (0. 8651±0. 4603, P＜0. 01 ). Treatedwith Allitridi, the patients' symptoms got improved and at the same time the filtering index of leucocytes lowered markedly(1. 6261±1. 3472). The conditions of the patients before and after treatments were obviously different(p＜0. 01). The index of the whole blood rheology was improved significantly. Conclusions: Allitridicould effectively improve the leucocytes deformation and the whole blood rheology as well, and alleviate clinicalsymptoms.
基金supported by the National Natural Science Foundation of China(No.81273516/No.81270222/No.81302779)Guangdong Provincial Natural Science Foundation(No.S2013010014762/No.S2013040014689)Guangdong Provincial Medical Science Foundation(No.A2011005/No.A2012006)
文摘Background Allitridi is an active compound that is extracted from the garlic. It has effects of anti-atherosclerosis, anti-arrhythmias and lowering blood pressure. But the controversy about the effect on cardiac contractility still exists. Methods Whole-cell patch clamp recording technique was used to record ICa,Lin single cell isolated rat ventricular myocytes. The nifedipine- sensitive L-type calcium current was recorded in the rat ventricular myocytes. Results Allitridi decreased the calcium channel current in a dose-dependent and voltage-dependent manner in ventricular myocytes of rats. The current-voltage curve was shifted upwards, on which active potential,peak potential and reverse potential showed no significant changes. The inactivation curve was shifted to more negative potential, but the activation curve and recovery curve were not altered. Allitridi had no effect on frequent-dependency of calcium current. Conclusion These results show that allitridi could concentration-dependently decrease calcium channel current in ventricular myocytes of rats.
文摘To exploring the effect of Allitridi on anti arrhythmia, cardiac electrophysiological characteristic are detected in guinea pig atrium muscles by intracellular microelectrode technique. Result:The automaticity which adrenalin induces is inhibited at 125 and 625 umol/L. The force of contraction is weakened; the intensity time curve which reflects excitability move towards right after 625 umol/L administration. under 25、125、625 μmol/L, functional refractory period、action potential duration of 50% and 90% repolarization、 sinus cycle longness are extended, a relationship between dose and effect exist at SCL. Conclusion: Automaticity、 excitability and refractoriness not only are inhibited but also action potential durations are extended after Allitridi administration.
