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1.南昌大学 第一附属医院,南昌 330006
2.江西省肿瘤医院,南昌 330029
3.江西中医药大学 中医学院,南昌 330004
侯本超,硕士,主治医师,从事肿瘤麻醉学的研究工作,E-mail:15236976@qq.com
刘海云,硕士,副教授,从事中药抗肿瘤的研究工作,E-mail:547906147@qq.com
收稿日期:2022-03-15,
网络出版日期:2022-06-30,
纸质出版日期:2023-03-05
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侯本超,何志坚,刘海云等.黄芪甲苷对结直肠癌HCT116细胞增殖、迁移及侵袭的影响[J].中国实验方剂学杂志,2023,29(05):144-149.
HOU Benchao,HE Zhijian,LIU Haiyun,et al.Effect of Astragaloside Ⅳ on Proliferation, Migration, and Invasion of Colorectal Cancer HCT116 Cells[J].Chinese Journal of Experimental Traditional Medical Formulae,2023,29(05):144-149.
侯本超,何志坚,刘海云等.黄芪甲苷对结直肠癌HCT116细胞增殖、迁移及侵袭的影响[J].中国实验方剂学杂志,2023,29(05):144-149. DOI: 10.13422/j.cnki.syfjx.20221728.
HOU Benchao,HE Zhijian,LIU Haiyun,et al.Effect of Astragaloside Ⅳ on Proliferation, Migration, and Invasion of Colorectal Cancer HCT116 Cells[J].Chinese Journal of Experimental Traditional Medical Formulae,2023,29(05):144-149. DOI: 10.13422/j.cnki.syfjx.20221728.
目的
2
探究黄芪甲苷对结直肠癌HCT116细胞增殖、迁移及侵袭能力的影响,并探讨其相关分子机制。
方法
2
将结直肠癌HCT116细胞分为空白组(DMSO)和黄芪甲苷低、中、高质量浓度组(15.7、31.4、62.8 mg·L
-1
)。通过倒置显微镜观察给药后结直肠癌HCT116细胞形态的改变;细胞增殖与活性检测-8(CCK-8)法检测黄芪甲苷处理后细胞活性的改变;细胞划痕实验和Transwell实验观察黄芪甲苷处理后结肠癌HCT116细胞迁移及侵袭能力的变化;蛋白免疫印迹法(Western blot)检测结直肠癌HCT16细胞周期蛋白依靠性激酶抑制剂(p21)、细胞周期蛋白D
1
(CyclinD
1
)及B细胞淋巴瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)表达水平。
结果
2
与空白组比较,黄芪甲苷低、中、高质量浓度组细胞生长速度慢,密度明显稀疏,细胞形态不一,细胞核逐渐缩小,细胞质逐渐降解,细胞死亡率高,细胞活力呈浓度依赖性下降,细胞迁移和侵袭能力明显受到抑制(
P
<
0.05,
P
<
0.01),其抑制率与给药浓度呈正相关;与空白组比较,黄芪甲苷低、中、高质量浓度组促凋亡蛋白Bax表达量逐渐升高,呈浓度依赖性,细胞周期蛋白p21、CyclinD
1
及抑制凋亡蛋白Bcl-2表达量逐渐降低(
P
<
0.05,
P
<
0.01),呈浓度依赖性。
结论
2
黄芪甲苷可抑制结直肠癌HCT116细胞的增殖、迁移和侵袭能力,促进细胞凋亡,从而抑制结直肠癌的发生发展。
Objective
2
To investigate effect of astragaloside Ⅳ on the proliferation, migration, and invasion of colorectal cancer HCT116 cells and the underlying molecular mechanism.
Method
2
Colorectal cancer HCT116 cells were classified into blank group (DMSO) and low-dose (15.7 mg·L
-1
), medium-dose (31.4 mg·L
-1
), and high-dose (62.8 mg·L
-1
) astragaloside Ⅳ groups. After drug treatment, the morphological changes of HCT116 cells were observed under an inverted microscope. Cell viability was detected by cell counting kit-8 (CCK-8) assay, and the migration and invasion of cells were detected based on scratch assay and Transwell assay. The expression of cyclin-dependent kinase inhibitor (p21), CyclinD
1
, B-cell lymphoma-2 (Bcl-2), and Bcl-2-associated X protein (Bax) in the cells was examined by Western blot.
Result
2
Compared with the blank group, cells in the three astragaloside Ⅳ groups demonstrated slow growth, low density, inconsistent morphology, nuclear shrinkage, degradation of cytoplasm, and high death rate. Moreover, cell viability decreased in a concentration-dependent manner in the astragaloside Ⅳ groups. Cell migration and invasion were inhibited (
P
<
0.05,
P
<
0.01), and the inhibition rate was in positive correlation with the concentration of the astragaloside Ⅳ. The expression of pro-apoptotic protein Bax in low-dose, medium-dose and high-dose astragaloside Ⅳ groups increased gradually in a concentration-dependent manner, while the expression of p21, CyclinD
1
and anti-apoptotic protein Bcl-2 decreased gradually in a concentration-dependent manner compared with those in the blank group (
P
<
0.05,
P
<
0.01).
Conclusion
2
Astragaloside Ⅳ can suppress the proliferation, migration, and invasion of colorectal cancer HCT116 cells and promote the apoptosis, thus inhibiting the occurrence and development of colorectal cancer.
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