马玉坤1,汤拓2,张鲁平2,孙珈1,郑皑雪2,洪鲜1,李静辉3,王涛1,洪瑜1▲.岩大戟内酯B对HeLa细胞增殖的影响及其凋亡机制研究[J].中国医药科学,2025,(5):13-16 基金项目:黑龙江省齐齐哈尔市科技计划联合引导项目(LSFGG-2022039);黑龙江省卫生健康委科研项目(20221313050620) |
岩大戟内酯B对HeLa细胞增殖的影响及其凋亡机制研究 |
Study on the effect of Jolkinolide B on HeLa cell proliferation and its apoptosis mechanism |
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DOI: |
中文关键词: 岩大戟内酯B;HeLa细胞;增殖;凋亡 |
英文关键词:Jolkinolide B; HeLa cell; Proliferation; Apoptosis |
作者 | 单位 | 马玉坤1,汤拓2,张鲁平2,孙珈1,郑皑雪2,洪鲜1,李静辉3,王涛1,洪瑜1▲ | 1.齐齐哈尔医学院医药科学研究院,黑龙江齐齐哈尔 161006;2.齐齐哈尔医学院医学技术学院,黑龙江齐齐哈尔 161006;3.齐齐哈尔医学院国有资产管理处,黑龙江齐齐哈尔 161006 |
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中文摘要: |
[摘要] 目的 研究岩大戟内酯B(JB)对宫颈癌(HeLa)细胞增殖与凋亡的影响及作用机制。 方法 将体外培养的HeLa细胞分为空白对照组和JB组(0.05、0.1、0.2、0.4 mmol/L),通过显微镜观察法、CCK-8实验法对经过JB处理的HeLa细胞的形态以及增殖能力进行检测,同时使用流式细胞技术荧光素5-异硫氰酸酯(FITC)、碘化丙啶双标法、蛋白质免疫印记法等方法对的细胞凋亡率及凋亡关键蛋白表达情况进行研究。 结果 与空白对照组比较,JB 在0.05~0.2 mmol/L范围内的细胞增殖抑制率显著增高(P < 0.05),且随JB浓度和处理时间的增加而显著提升;JB 0.05~0.2 mmol/L组的相关蛋白表达量Caspase-3、Bax显著上调(P < 0.05)而PCNA、Bcl-2显著下调(P < 0.05)。 结论 JB能有效抑制HeLa细胞增殖,实现其诱导细胞凋亡的作用,该机制可能和参与调控HeLa细胞增殖与凋亡的相关蛋白表达密切相关,JB刺激HeLa细胞能够通过加重炎症反应从而促进癌症细胞凋亡的发生发展,进而抑制HeLa细胞的增殖能力。 |
英文摘要: |
[Abstract] Objective To study the effect and mechanism of Jolkinolide B (JB) on the proliferation and apoptosis of cervical cancer (HeLa) cells. Methods HeLa cells cultured in vitro were divided into blank control group and JB group (0.05, 0.1, 0.2, 0.4 mmol/L). The morphology and proliferation ability of HeLa cells treated with JB were detected by microscopic observation and CCK-8 experiment. Flow cytometry techniques such as fluorescein 5-isothiocyanate (FITC), propidium iodide double staining, and Western blot were used to study the apoptosis rate and expression of key apoptotic proteins. Results Compared with the control group, the cell proliferation inhibition rate of JB was significantly increased within the range of 0.05-0.2 mmol/L (P < 0.05), and significantly increased with the increase of JB concentration and treatment time. The protein expression levels of Caspase-3 and Bax were significantly upregulated (P < 0.05) in the JB 0.05-0.2 mmol/L group, while PCNA and Bcl-2 were significantly downregulated (P < 0.05). Conclusion JB can effectively inhibit the proliferation of HeLa cells and induce cell apoptosis. This mechanism may be closely related to the expression of related proteins involved in regulating HeLa cell proliferation and apoptosis. JB stimulation of HeLa cells can promote the occurrence and development of cancer cell apoptosis by exacerbating the inflammatory response, thereby inhibiting the proliferation ability of HeLa cells. |
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