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作 者:刘迎雪 贾秀红[1] 伊英杰[1] 朱聪[1] Liu Yingxue;Jia Xiuhong;Yi Yingiie;Zhu Cong(Department of Pediatrics,the Affiliated Hospital of Binzhou Medical University,Binzhou 256603,Shandong Province,China)
出 处:《中华实用儿科临床杂志》2018年第21期1649-1651,共3页Chinese Journal of Applied Clinical Pediatrics
基 金:山东省自然科学基金(ZR2014HL032);山东省医药卫生科技发展项目(2014WS0183)
摘 要:目的探讨龙葵碱对急性T淋巴细胞白血病(T-ALL)Jurkat细胞增殖、凋亡的作用及其机制。方法采用不同质量浓度龙葵碱分别处理Jurkat细胞24、48、72 h后,通过CCK-8法观察龙葵碱对Jurkat细胞增殖的影响,通过流式细胞术检测龙葵碱对Jurkat细胞凋亡的影响,不同浓度龙葵碱处理Jurkat细胞后,Western blot法检测Bcl-2和Bax的表达;并通过实时荧光定量聚合酶链反应(qPCR)技术检测Bcl-2 mRNA和Bax mRNA的表达水平。结果CCK-8结果显示:龙葵碱显著抑制Jurkat细胞增殖,并呈剂量和时间依赖性;流式细胞术检测凋亡结果显示:0、4、16 mg/L的龙葵碱处理Jurkat细胞24 h后,细胞的凋亡比例分别为(2.40±0.98)%、(28.43±4.86)%、(41.56±1.87)%,呈剂量依赖性。Western blot结果显示:龙葵碱在Jurkat细胞中能增加Bax表达,降低Bcl-2表达,均呈剂量依赖性。结论龙葵碱能显著抑制Jurkat细胞株的增殖,诱导其凋亡,其机制与上调Bax表达及下调Bcl-2表达有关。ObjectiveTo explore the effect of proliferation and apoptosis of Solanine on acute T lymphocyte leukemia (T-ALL) Jurkat cells and its mechanism.MethodsAfter treated with different concentrations of Solanine, the proliferation of Jurkat cells was detected by CCK-8 assay, and the effect of Solanine on apoptosis of Jurkat cells were detected by flow cytometry.The expression of Bcl-2 and Bax in Jurkat cells were detected by Western blot, and the expression levels of Bcl-2 mRNA and Bax mRNA were detected by real-time fluorescence quantitative polyme-rase chain reaction.ResultsCCK-8 assay showed that Solanine significantly inhibited the proliferation of Jurkat cells in a dose-and time-dependent manner. The results of flow cytometry showed that the apoptosis rates of Jurkat cells treated with Solanine for 24 h were (2.40±0.98)%, (28.43±4.86)%, (41.56±1.87)%, respectively, in a dose-dependent manner. Western blot showed that Solanine could increase the expression of Bax and decrease the expression of Bcl-2 in Jurkat cells, and they all were dose-dependent.ConclusionSolanine can significantly inhibit the proliferation and induce apoptosis of Jurkat cells. The mechanism is related to the up-regulation of Bax expression and down-regulation of Bcl-2 expression.
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