首页|雷公藤红素对人食管鳞癌KYSE180细胞增殖、凋亡的影响及其作用机制

雷公藤红素对人食管鳞癌KYSE180细胞增殖、凋亡的影响及其作用机制

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目的 分析雷公藤红素对人食管鳞癌KYSE180细胞增殖、凋亡的影响,并探讨其可能的作用机制.方法 取对数生长期KYSE180细胞,分别加入0.5、1、2μmol/L的雷公藤红素,同时设空白对照组.MTT法和克隆形成试验检测细胞的增殖情况;流式细胞术检测细胞的凋亡情况;Transwell小室试验检测细胞的迁移及侵袭能力;qRT-PCR法检测细胞中P53、FAS、DR5基因mRNA的转录水平;Western blot法检测细胞中Caspase-3、Caspase-9、Bax、Bcl-2、PARP蛋白的表达水平.结果 与空白对照组比较,2μmol/L雷公藤红素组细胞增殖明显受到抑制(F=10.9,P<0.05),0.5、1 μmol/L雷公藤红素组克隆数明显减少(F=457.9,P<0.05);1、2 μmol/L雷公藤红素组细胞的侵袭和迁移数量明显下降(F=751.7~1 134.0,P均<0.001);0.5、1、2 μmol/L雷公藤红素组细胞凋亡率明显升高(F=243.0~728.0,P均<0.05);1及2 μmol/L雷公藤红素组细胞中P53、FAS、DR5基因mRNA转录水平显著提高(F=71.0~539.3,P均<0.01);1、2 μmol/L雷公藤红素组Cspase-3、Caspase-9、Bax蛋白表达水平明显增加(F分别为 142.1、35.3、347.6,P 均<0.01),2 μmol/L 雷公藤红素组 PARP 蛋白水平明显增加(F=877.6,P<0.01),0.5、1、2 μmol/L雷公藤红素组Bcl-2蛋白表达明显下降(F=59.2,P均<0.01).结论 雷公藤红素可抑制KYSE180细胞的增殖、促进凋亡,可能是通过上调Caspase-3/9、Bax、PARP蛋白的表达,下调Bcl-2蛋白的表达而发挥作用.
Effect of celastrol on proliferation and apoptosis of human esophageal squamous cell carcinoma KYSE180 cells and its mechanism
Objective To explore the effect of celastrol on the proliferation and apoptosis of human esophageal squamous cell carcinoma KYSE180 cells and the possible mechanism.Methods KYSE180 cells in logarithmic growth phase were added with 0.5,1 and 2 μmol/L of celastrol respectively,and the blank control group was set up.MTT assay and colony formation test were used to detect the proliferation of cells;the apoptosis of cells was assessed by flow cytometry;Transwell assay was used to measure the migration and invasion ability of cells;the mRNA transcription levels of P53,FAS and DR5 were determined by qRT-PCR;the expression levels of Caspase-3,Caspase-9,Bax,Bcl-2 and PARP proteins were detected by Western blot.Results Compared with the control group,cell proliferation in 2 μmol/L celastrol group was significantly inhibited(F=10.9,P<0.05),and the numbers of clones in 0.5 and 1 μmol/L celastrol groups decreased significantly(F=457.9,P<0.05);the numbers of cell invasion and migration decreased significantly in 1 and 2 μmol/L celastrol groups(F=751.7-1 134.0,each P<0.001);the apoptosis rates in 0.5,1 and 2 μmol/L celastrol groups increased signifi-cantly(F=243.0-728.0,each P<0.05);the mRNA transcription levels of P53,FAS and DR5 in 1 and 2 μmol/L celastrol groups significantly increased(F=71.0-539.3,each P<0.01);the protein expression levels of Caspase-3,Cas-pase-9 and Bax in 1 and 2 μmol/L celastrol groups significantly increased(F=142.1,35.3 and 347.6,respectively,each P<0.01),the level of PARP in 2 μmol/L celastrol group significantly increased(F=877.6,P<0.01),and the expression of Bcl-2 in 0.5,1 and 2 μmol/L celastrol groups decreased significantly(F=59.2,each P<0.01).Conclusion Celastrol can inhibit the proliferation and promote the apoptosis of KYSE180 cells,probably through the up-regulation of Caspase-3/9,Bax,PARP protein expression and the down-regulation of Bcl-2 protein expression.

CelastrolEsophageal squamous cell carcinomaProliferationApoptosis

李香、马燕春、张宇涵、花雨艳、成晓龙

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山西医科大学食管癌转化研究中心,山西太原 030000

雷公藤红素 食管鳞癌 细胞增殖 细胞凋亡

国家自然科学基金山西省自然科学基金

81802440201801D221400

2024

中国生物制品学杂志
中华预防医学会,长春生物制品研究所有限责任公司

中国生物制品学杂志

CSTPCD
影响因子:0.417
ISSN:1004-5503
年,卷(期):2024.37(4)
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