中国药物经济学2024,Vol.19Issue(8) :111-116,125.DOI:10.12010/j.issn.1673-5846.2024.08.024

榄绿粗叶木乙酸乙酯提取物通过IL-24/Bcl-2通路诱导肝癌细胞凋亡的机制

The Mechanism of Hepatocellular Carcinoma Cell Apoptosis Induced by Ethyl Acetate Extract of Oliva Virifolia via IL-24/Bcl-2 Pathway

谢永华 温扬敏
中国药物经济学2024,Vol.19Issue(8) :111-116,125.DOI:10.12010/j.issn.1673-5846.2024.08.024

榄绿粗叶木乙酸乙酯提取物通过IL-24/Bcl-2通路诱导肝癌细胞凋亡的机制

The Mechanism of Hepatocellular Carcinoma Cell Apoptosis Induced by Ethyl Acetate Extract of Oliva Virifolia via IL-24/Bcl-2 Pathway

谢永华 1温扬敏1
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作者信息

  • 1. 泉州医学高等专科学校基础医学部,福建泉州 362011
  • 折叠

摘要

目的 探讨榄绿粗叶木乙酸乙酯提取物(EE-LLA)通过IL-24/Bcl-2 通路诱导肝癌细胞凋亡的机制.方法 CCK8方法检测EE-LLA对小鼠肝癌H22 细胞增殖的影响;流式细胞检测EE-LLA对小鼠肝癌H22 细胞的影响;qPCR检测各组细胞中IL-24 和Bcl-2 基因表达水平;Western blot检测各组细胞中IL-24 和Bcl-2 蛋白表达水平.结果 随着EE-LLA浓度的逐步升高以及作用时间的延长,小鼠肝癌 H22 细胞的增殖率呈显著下降趋势,与对照组比较差异有统计学意义(P<0.05).EE-LLA作用H22 细胞24 h,细胞半数抑制浓度(IC50)为0.91 mg/ml,48 h,IC50 为0.72 mg/ml,72 h,IC50 为0.75 mg/ml.与对照组相比,不同浓度EE-LLA分别作用小鼠肝癌H22 细胞48 h,小鼠肝癌H22 细胞的IL-24 mRNA表达量升高,Bcl-2 mRNA表达量降低,差异有统计学意义(P<0.05),且具有一定的浓度依赖性;与对照组相比,不同浓度(1.2、2.4、4.8 mg/ml)的EE-LLA分别作用48 h后,小鼠肝癌H22 细胞的IL-24 蛋白表达量增加,Bcl-2 蛋白表达量降低,差异有统计学意义(P<0.05).结论 EE-LLA 对小鼠肝癌 H22 细胞增殖具有显著抑制效果,其潜在机制可能涉及上调 IL-24基因的表达并伴随Bcl-2 基因表达的下调,这一双重调控作用进而触发了肿瘤细胞的凋亡过程.

Abstract

Objective To explore the mechanism of hepatocellular carcinoma cell apoptosis induced by ethyl acetate extract(EE-LLA)through IL-24/Bcl-2 pathway.Methods The effect of EE-LLA on the proliferation of mouse liver cancer H22 cells was detected by CCK8.The effect of EE-LLA on mouse liver cancer H22 cells was detected by flow cytometry.The gene expression levels of IL-24 and Bcl-2 in each group were detected by qPCR.The protein expression levels of IL-24 and Bcl-2 in each group were detected by Western blot.Results As the concentration of EE-LLA gradually increased and the duration of exposure was extended,the proliferation rate of mouse liver cancer H22 cells exhibited a significant downward trend,with a statistically significant difference compared to the control group(P<0.05).The IC50 of EE-LLA on H22 cells was 0.91 mg/mlat 24 h,0.72 mg/ml at 48 h and 0.75 mg/ml at 72 h.Compared with the control group,different concentrations of EE-LLA treated mouse hepatocellular carcinoma H22 cells for 48 h,the expression of IL-24 mRNA increased,and the expression of Bcl-2 mRNA decreased,the difference was statistically significant(P<0.05),and there was a certain concentration dependence;the expression of IL-24 protein was increased in H22 cells,while the expression of Bcl-2 protein was decreased,the difference was statistically significant(P<0.05).Conclusion EE-LLA can inhibit the proliferation of mouse liver cancer H22 cells,and its mechanism may be to up-regulate the expression of IL-24 gene and down-regulate the expression of Bcl-2 gene,thereby inducing tumor cell apoptosis.

关键词

榄绿粗叶木乙酸乙酯提取物/肝癌/IL-24/Bcl-2

Key words

Lasianthus lancilimbus extracted by ethyl acetate/Hepatoma/IL-24/Bcl-2

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基金项目

福建省中青年教师教育科研项目(JAT201239)

出版年

2024
中国药物经济学
中国中医药研究促进会

中国药物经济学

影响因子:0.712
ISSN:1673-5846
参考文献量8
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