Molecular Mechanism of Fuzheng Kang'ai Decoction in Inducing Apoptosis of H1650 Cells

LI Long-mei; WU Wan-yin; WANG Su-mei; LONG Shun-qin; YANG Xiao-bing; ZHOU Yu-shu

doi:10.13422/j.cnki.syfjx.2016140106

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Molecular Mechanism of Fuzheng Kang'ai Decoction in Inducing Apoptosis of H1650 Cells

更新时间：2024-01-04

- Molecular Mechanism of Fuzheng Kang'ai Decoction in Inducing Apoptosis of H1650 Cells
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 22, Issue 14, Pages: 106-110(2016)
- 作者机构：
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2016140106
  CLC： R285
- Published：2016
- 稿件说明：
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LI Long-mei, WU Wan-yin, WANG Su-mei, et al. Molecular Mechanism of Fuzheng Kang'ai Decoction in Inducing Apoptosis of H1650 Cells[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(14): 106-110.
DOI：

LI Long-mei, WU Wan-yin, WANG Su-mei, et al. Molecular Mechanism of Fuzheng Kang'ai Decoction in Inducing Apoptosis of H1650 Cells[J]. Chinese journal of experimental traditional medical formulae, 2016, 22(14): 106-110. DOI： 10.13422/j.cnki.syfjx.2016140106.

摘要

目的：观察扶正抗癌方对H1650细胞凋亡的影响，并探讨其诱导H1650细胞凋亡的分子机制。方法：以人肺腺癌细胞株H1650细胞为研究对象，用0.5，1.0，1.5，2.0，2.5，3.0g·L-1扶正抗癌方处理H1650细胞24，48，72h，另设空白组，四氮唑蓝盐化合物（MTS）法检测细胞增殖；用0.5，1.0，1.5g·L-1扶正抗癌方处理H1650细胞24h，另设空白组，AnnexinV-FITC/碘化丙啶（PI）流式细胞术检测细胞凋亡；用0.5，1.0，2.0g·L-1扶正抗癌方处理H1650细胞24h，另设空白组，半胱氨酸蛋白酶-3/7（Caspase-3/7）活力检测试剂盒检测Caspase-3/7活力；蛋白免疫印迹法检测扶正抗癌方对proCasapse-3，聚腺苷二磷酸-核糖聚合酶（PARP），Bcl-2相关X蛋白（Bax）表达。结果：与空白组比较，扶正抗癌方能明显抑制H1650细胞的增殖（P<0.05），且呈浓度和时间依赖性。与空白组比较，扶正抗癌方明显诱导H1650细胞的早期凋亡，增强Caspase-3/7的活力（P<0.05），且呈浓度依赖性。与空白组比较，扶正抗癌方明显下调proCasapse-3和PARP的表达（P<0.05），呈浓度依赖性，明显上调Bax的表达（P<0.05），且呈时间依赖性。结论：扶正抗癌方可通过激活Caspase-3和Bax诱导H1650细胞的凋亡。

Abstract

Objective: To observe the effects of Fuzheng Kang'ai (FZKA) decoction on apoptosis of H1650 cells and discuss its molecular mechanism in apoptosis of H1650 cells. Method: Human lung adenocarcinoma cells (H1650 cells) were used as the research objects and treated for 24

72 h with 0.5

1.0

1.5

2.0

2.5

3.0 g · L-1 FZKA decoction

and a blank group was set up

then cell proliferation was detected by 3- (4

5-diethylthiazol-2-yl)-5- (3-carboxymethoxyphenyl)-2- (4-sulfophenyl)-2H-etrazolium

inner salt (MTS) assay. H1650 cells were treated for 24 h with 0.5

1.0

1.5 g · L-1 FZKA decoction and a blank group was set up

then cell apoptosis was detected by Annexin V-FITC/PI flow cytometry analysis. H1650 cells were treated for 24 h with 0.5

1.0

2.0 g · L-1 FZKA decoction and a blank group was set up

then vitality of Caspase-3/7 was detected by Caspase-3/7 vitality test kit. Simultaneously

effects of FZKA decoction on the expression levels of proCasapse-3

PARP and Bax were detected by Western blot assay. Result: As compared with the blank group

proliferation of H1650 cells was significantly inhibited by FZKA decoction in concentration-dependent and time-dependent manners (P<0.05). As compared with the blank group

early apoptosis of H1650 cells was significantly induced and vitality of Caspase-3/7 was increased by FZKA decoction in a concentration-dependent manner (P<0.05). As compared with the blank group

the expression levels of proCasapse-3 and PARP were significantly reduced by FZKA decoction in a concentration-dependent manner (P<0.05)

and the expression of Bax was increased by FZKA decoction in a time-dependent manner (P<0.05). Conclusion: Apoptosis is induced by FZKA decoction in way of activating Caspase-3 and Bax in H1650 cells.

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