首页> 中文期刊> 《实用临床医药杂志》 >β-咔啉类生物碱对人胃癌细胞SGC-7901增殖的影响

β-咔啉类生物碱对人胃癌细胞SGC-7901增殖的影响

         

摘要

目的:探讨β-咔啉类生物碱对人胃癌细胞 SGC-7901增殖的影响。方法通过体外培养人胃癌细胞株 SGC-7901,将含有不同浓度(5、10、20、40μg/mL)β-咔啉类生物碱的培养液与 SGC-7901细胞共同培养24 h 和48 h。采用 MTT 比色法计算细胞抑制率;在荧光显微镜下用 Hoechst 33258细胞核染色法观察细胞形态学改变;流式细胞仪检测凋亡率及基因组DNA 琼脂凝胶电泳检测凋亡梯状条带。结果β-咔啉类生物碱对 SGC-7901细胞的损伤呈浓度依赖性;β-咔啉类生物碱分别作用24 h 和48 h 后半数抑制浓度(IC50)分别为17.79μg/mL 和12.17μg/mL;荧光染色可观察到有细胞核固缩及核断裂的凋亡现象;流式细胞术显示:阴性对照组(0μg/mL)及β-咔啉类生物碱5、10、20、40μg/mL 浓度组24、48 h 凋亡率为别1.66%、11.27%、20.32%、30.66%、41.42%和3.84%、15.29%、23.34%、34.87%、49.54%,细胞凋亡率伴随给药浓度增加而增加;基因组 DNA 琼脂糖凝胶电泳检测到明显的凋亡梯状条带。结论β-咔啉类生物碱能诱导人胃癌 SGC-7901细胞发生凋亡,抑制细胞增殖。%Objective To investigate the effects of β-Carboline of alkaloids on proliferation of SGC-7901 of human gastric cancer cells.Methods SGC-7901 cells were cultured in vitro initially. After SGC-7901 cells were incubated with β-Carboline alkaloids at different concentrations of 5,10, 20,40 μg/mL for 24,48 hours,the inhibited proliferation rate of SGC-7901 cells were examined by Methtl Thiazolyl Tetrazolium(MTT)assay.Morphological changes of SGC-7901 cells were observed by Hoechst 33258 under fluorescence microscope.Flow cytometry was used to detect cell apoptosis after SGC-7901 cells were incubated with β-Carboline alkaloids for 24 hours.Cell gemonic DNA was detec-ted by agarose electrophoresis.Results β-Carboline of alkaloids induced damage of SGC-7901 cell in a concentration dependent manner .The IC 5 0 of β-Carboline alkaloids at 2 4 ,4 8 hours were 17.79 μg/mL and 12.17 μg/mL respectively.Apoptotic cells were observed and flow cytonetry analy-sis in dicated that the apoptosis rate of cells treated with different concentrations of β-Carboline alka-loids(0,5,10,20,40 μg/mL)for 24 and 48 hours were 1.66%,11.27%,20.32%,30.66%, 41.42%;3.84%,15.29%,23.34%,34.87%,49.54%,respectively.Increasing in apoptosis rate of SGC-7901 cells was associated with drug concentration.Typical DNA Ladder was detected in DNA agarose electrophoresis.Conclusion β-Carboline alkaloids can inhibit the proliferation and in-duce the apoptosis of SGC-7901 cells.

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