羧甲基-&beta;-1,3-葡聚糖对人肝癌HepG2细胞的放射增敏作用

马斌博; 王转子; 魏巍; 党秉荣; 李文建

doi:10.11804/NuclPhysRev.34.04.797

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羧甲基-β-1,3-葡聚糖对人肝癌HepG2细胞的放射增敏作用

马斌博, 王转子, 魏巍, 党秉荣, 李文建

文章导航 > 原子核物理评论 > 2017 > 34(4): 797-802

马斌博, 王转子, 魏巍, 党秉荣, 李文建. 羧甲基-β-1,3-葡聚糖对人肝癌HepG2细胞的放射增敏作用[J]. 原子核物理评论, 2017, 34(4): 797-802. doi: 10.11804/NuclPhysRev.34.04.797

引用本文:

MA Binbo, WANG Zhuanzi, WEI Wei, DANG Bingrong, LI Wenjian. Effects of Carboxymethy-β-1,3-glucan on Human Hepatoma HepG2 Cells Radiosensitivity[J]. Nuclear Physics Review, 2017, 34(4): 797-802. doi: 10.11804/NuclPhysRev.34.04.797

Citation:

MA Binbo, WANG Zhuanzi, WEI Wei, DANG Bingrong, LI Wenjian. Effects of Carboxymethy-β-1,3-glucan on Human Hepatoma HepG2 Cells Radiosensitivity[J]. Nuclear Physics Review, 2017, 34(4): 797-802. doi: 10.11804/NuclPhysRev.34.04.797

羧甲基-β-1,3-葡聚糖对人肝癌HepG2细胞的放射增敏作用

doi: 10.11804/NuclPhysRev.34.04.797

1.
中国科学院近代物理研究所, 兰州 730000;
2.
兰州大学, 兰州 730000

基金项目: 国家自然科学基金资助项目（11575259）

详细信息

作者简介:
马斌博(1987-),男,甘肃白银人,硕士研究生,从事辐射增敏与防护药物研究;E-mail:mabb13@lzu.edu.cn.

通讯作者: 李文建,E-mail:wjli@impcas.ac.cn。

中图分类号: R730.55;R96

Effects of Carboxymethy-β-1,3-glucan on Human Hepatoma HepG2 Cells Radiosensitivity

1.
Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China;
2.
Lanzhou University, Lanzhou 730000, China

Funds: National Natural Science Foundation of China(11575259)

摘要: 本研究旨在探讨羧甲基-β-1，3葡聚糖（CMG）对人肝癌HepG2细胞X射线或¹²C⁶⁺离子束辐射敏感性的影响。首先用CCK-8法检测CMG对HepG2细胞的生长抑制情况，得到半数抑制浓度（IC50）为120.6μg/mL。用浓度为0.1×IC50的CMG预处理HepG2细胞24 h，再给予2 Gy X射线或¹²C⁶⁺离子束辐照（CMG+辐照组）；CMG未处理组直接接受2 Gy X射线或¹²C⁶⁺离子束辐照（辐照组）。对比分析辐照组和CMG+辐照组细胞的克隆存活、DNA损伤、凋亡与周期分布、细胞内活性氧（ROS）水平。发现：与X射线辐照组相比，相同剂量的¹²C⁶⁺离子辐照组克隆存活率更小，DNA损伤和周期阻滞更加严重，细胞凋亡率和细胞内ROS水平也更高。与单独X射线或¹²C⁶⁺离子束辐照组相比，CMG+辐照组克隆存活率明显降低，细胞凋亡率随辐照后CMG作用时间的延长而明显增加，CMG使辐照后细胞内ROS维持在一个较高的水平，同时CMG明显加重了单独辐照诱导的DNA损伤和周期阻滞。结果表明，与X射线相比，HepG2细胞对相同剂量的¹²C⁶⁺离子辐射更敏感；CMG可增加HepG2细胞对X射线或¹²C⁶⁺离子辐射的敏感性；CMG可能通过增加受照HepG2细胞内的ROS水平，加剧辐照诱导的DNA损伤，促进辐射诱导细胞凋亡而起到辐射增敏作用。

This study aims to investigate the effect of carboxymethy-β-1, 3-glucan (CMG) on the sensitivity of human hepatoma HepG2 cells to X-rays or ¹²C⁶⁺ ions irradiation. First, the inhibitory effect of CMG on the growth of HepG2 cells was detected by CCK-8 assay, and the half maximal inhibitory concentration (IC50) was 120.6 μg/mL. HepG2 cells were pretreated with CMG at a concentration of 0.1×IC50 for 24 h and then irradiated with 2 Gy X-ray or ¹²C⁶⁺ ion beams (CMG + irradiation group). CMG untreated group was directly irradiated by 2 Gy X-rays or ¹²C⁶⁺ ions beam (irradiation group). The clone survival, DNA damage, cell apoptosis, cell cycle distribution, and intracellular reactive oxygen species (ROS) levels in irradiation group and CMG + irradiation group were comparatively analyzed. The results showed that the clone survival rate was lower, DNA damage and cycle arrest were more serious, and the rate of apoptosis and intracellular ROS levels were higher in ¹²C⁶⁺ ions irradiation group than those in the same dose of X-rays irradiation group. Compared with X-rays or ¹²C⁶⁺ ions irradiation group, the clone survival rate of CMG + irradiation group was significantly decreased, and the apoptosis rate significantly increased with the prolongation of CMG treatment post-irradiation; CMG maintained intracellular ROS at a higher level after irradiation, CMG also significantly aggravated radiation-induced DNA damage and cycle arrest. These results indicated that HepG2 cells were more sensitive to ¹²C⁶⁺ ions radiation than those at the same dose of X-rays. CMG increased the sensitivity of HepG2 cells to X-rays or ¹²C⁶⁺ ions irradiation by increasing intracellular ROS level, exacerbating radiation-induced DNA damage and promoting radiation-induced apoptosis in irradiated HepG2 cells.
- 羧甲基-&beta /
- -1,3-葡聚糖 /
- HepG2细胞 /
- X射线辐照 /
- ¹²C⁶⁺离子辐照 /
- 辐射敏感性
Abstract: This study aims to investigate the effect of carboxymethy-β-1, 3-glucan (CMG) on the sensitivity of human hepatoma HepG2 cells to X-rays or ¹²C⁶⁺ ions irradiation. First, the inhibitory effect of CMG on the growth of HepG2 cells was detected by CCK-8 assay, and the half maximal inhibitory concentration (IC50) was 120.6 μg/mL. HepG2 cells were pretreated with CMG at a concentration of 0.1×IC50 for 24 h and then irradiated with 2 Gy X-ray or ¹²C⁶⁺ ion beams (CMG + irradiation group). CMG untreated group was directly irradiated by 2 Gy X-rays or ¹²C⁶⁺ ions beam (irradiation group). The clone survival, DNA damage, cell apoptosis, cell cycle distribution, and intracellular reactive oxygen species (ROS) levels in irradiation group and CMG + irradiation group were comparatively analyzed. The results showed that the clone survival rate was lower, DNA damage and cycle arrest were more serious, and the rate of apoptosis and intracellular ROS levels were higher in ¹²C⁶⁺ ions irradiation group than those in the same dose of X-rays irradiation group. Compared with X-rays or ¹²C⁶⁺ ions irradiation group, the clone survival rate of CMG + irradiation group was significantly decreased, and the apoptosis rate significantly increased with the prolongation of CMG treatment post-irradiation; CMG maintained intracellular ROS at a higher level after irradiation, CMG also significantly aggravated radiation-induced DNA damage and cycle arrest. These results indicated that HepG2 cells were more sensitive to ¹²C⁶⁺ ions radiation than those at the same dose of X-rays. CMG increased the sensitivity of HepG2 cells to X-rays or ¹²C⁶⁺ ions irradiation by increasing intracellular ROS level, exacerbating radiation-induced DNA damage and promoting radiation-induced apoptosis in irradiated HepG2 cells.
- carboxymethy-&beta /
- -1,3-glucan /
- HepG2 cells /
- X-rays irradiation /
- ¹²C⁶⁺ions irradiation /
- radiosensitivity

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[2]	ZHOU X, ZHANG X, XIE Y, et al. Plos One, 2013, 8(8):e72641.
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[4]	KEENAN J M, GOULSON M, SHAMLIYAN T, et al. British Journal of Nutrition, 2007, 97(6):1162.
[5]	SMITH K N, QUEENAN K M, THOMAS W, et al. Journal of the American College of Nutrition, 2008, 27(3):434.
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羧甲基-β-1,3-葡聚糖对人肝癌HepG2细胞的放射增敏作用

doi: 10.11804/NuclPhysRev.34.04.797

1. 中国科学院近代物理研究所, 兰州 730000;

2. 兰州大学, 兰州 730000

基金项目: 国家自然科学基金资助项目（11575259）

作者简介:
马斌博(1987-),男,甘肃白银人,硕士研究生,从事辐射增敏与防护药物研究;E-mail:mabb13@lzu.edu.cn.

通讯作者: 李文建,E-mail:wjli@impcas.ac.cn。

收稿日期: 2016-12-28
修回日期: 2017-01-10
刊出日期: 2017-12-20

中图分类号: R730.55;R96

关键词:

HepG2细胞 /

¹²C⁶⁺离子辐照 /

摘要: 本研究旨在探讨羧甲基-β-1，3葡聚糖（CMG）对人肝癌HepG2细胞X射线或¹²C⁶⁺离子束辐射敏感性的影响。首先用CCK-8法检测CMG对HepG2细胞的生长抑制情况，得到半数抑制浓度（IC50）为120.6μg/mL。用浓度为0.1×IC50的CMG预处理HepG2细胞24 h，再给予2 Gy X射线或¹²C⁶⁺离子束辐照（CMG+辐照组）；CMG未处理组直接接受2 Gy X射线或¹²C⁶⁺离子束辐照（辐照组）。对比分析辐照组和CMG+辐照组细胞的克隆存活、DNA损伤、凋亡与周期分布、细胞内活性氧（ROS）水平。发现：与X射线辐照组相比，相同剂量的¹²C⁶⁺离子辐照组克隆存活率更小，DNA损伤和周期阻滞更加严重，细胞凋亡率和细胞内ROS水平也更高。与单独X射线或¹²C⁶⁺离子束辐照组相比，CMG+辐照组克隆存活率明显降低，细胞凋亡率随辐照后CMG作用时间的延长而明显增加，CMG使辐照后细胞内ROS维持在一个较高的水平，同时CMG明显加重了单独辐照诱导的DNA损伤和周期阻滞。结果表明，与X射线相比，HepG2细胞对相同剂量的¹²C⁶⁺离子辐射更敏感；CMG可增加HepG2细胞对X射线或¹²C⁶⁺离子辐射的敏感性；CMG可能通过增加受照HepG2细胞内的ROS水平，加剧辐照诱导的DNA损伤，促进辐射诱导细胞凋亡而起到辐射增敏作用。

This study aims to investigate the effect of carboxymethy-β-1, 3-glucan (CMG) on the sensitivity of human hepatoma HepG2 cells to X-rays or ¹²C⁶⁺ ions irradiation. First, the inhibitory effect of CMG on the growth of HepG2 cells was detected by CCK-8 assay, and the half maximal inhibitory concentration (IC50) was 120.6 μg/mL. HepG2 cells were pretreated with CMG at a concentration of 0.1×IC50 for 24 h and then irradiated with 2 Gy X-ray or ¹²C⁶⁺ ion beams (CMG + irradiation group). CMG untreated group was directly irradiated by 2 Gy X-rays or ¹²C⁶⁺ ions beam (irradiation group). The clone survival, DNA damage, cell apoptosis, cell cycle distribution, and intracellular reactive oxygen species (ROS) levels in irradiation group and CMG + irradiation group were comparatively analyzed. The results showed that the clone survival rate was lower, DNA damage and cycle arrest were more serious, and the rate of apoptosis and intracellular ROS levels were higher in ¹²C⁶⁺ ions irradiation group than those in the same dose of X-rays irradiation group. Compared with X-rays or ¹²C⁶⁺ ions irradiation group, the clone survival rate of CMG + irradiation group was significantly decreased, and the apoptosis rate significantly increased with the prolongation of CMG treatment post-irradiation; CMG maintained intracellular ROS at a higher level after irradiation, CMG also significantly aggravated radiation-induced DNA damage and cycle arrest. These results indicated that HepG2 cells were more sensitive to ¹²C⁶⁺ ions radiation than those at the same dose of X-rays. CMG increased the sensitivity of HepG2 cells to X-rays or ¹²C⁶⁺ ions irradiation by increasing intracellular ROS level, exacerbating radiation-induced DNA damage and promoting radiation-induced apoptosis in irradiated HepG2 cells.

English Abstract

Effects of Carboxymethy-β-1,3-glucan on Human Hepatoma HepG2 Cells Radiosensitivity

1. Institute of Modern Physics, Chinese Academy of Sciences, Lanzhou 730000, China;

2. Lanzhou University, Lanzhou 730000, China

Funds: National Natural Science Foundation of China(11575259)

Received Date: 2016-12-28
Rev Recd Date: 2017-01-10
Publish Date: 2017-12-20

Keywords:

Abstract: This study aims to investigate the effect of carboxymethy-β-1, 3-glucan (CMG) on the sensitivity of human hepatoma HepG2 cells to X-rays or ¹²C⁶⁺ ions irradiation. First, the inhibitory effect of CMG on the growth of HepG2 cells was detected by CCK-8 assay, and the half maximal inhibitory concentration (IC50) was 120.6 μg/mL. HepG2 cells were pretreated with CMG at a concentration of 0.1×IC50 for 24 h and then irradiated with 2 Gy X-ray or ¹²C⁶⁺ ion beams (CMG + irradiation group). CMG untreated group was directly irradiated by 2 Gy X-rays or ¹²C⁶⁺ ions beam (irradiation group). The clone survival, DNA damage, cell apoptosis, cell cycle distribution, and intracellular reactive oxygen species (ROS) levels in irradiation group and CMG + irradiation group were comparatively analyzed. The results showed that the clone survival rate was lower, DNA damage and cycle arrest were more serious, and the rate of apoptosis and intracellular ROS levels were higher in ¹²C⁶⁺ ions irradiation group than those in the same dose of X-rays irradiation group. Compared with X-rays or ¹²C⁶⁺ ions irradiation group, the clone survival rate of CMG + irradiation group was significantly decreased, and the apoptosis rate significantly increased with the prolongation of CMG treatment post-irradiation; CMG maintained intracellular ROS at a higher level after irradiation, CMG also significantly aggravated radiation-induced DNA damage and cycle arrest. These results indicated that HepG2 cells were more sensitive to ¹²C⁶⁺ ions radiation than those at the same dose of X-rays. CMG increased the sensitivity of HepG2 cells to X-rays or ¹²C⁶⁺ ions irradiation by increasing intracellular ROS level, exacerbating radiation-induced DNA damage and promoting radiation-induced apoptosis in irradiated HepG2 cells.