| 刘皎皎,李粉萍,杨跃青,等.白花蛇舌草提取物对肝癌细胞 JNK/p38MARK通路及细胞学行为的影响[J].安徽医药,2022,26(8):1496-1500. |
| 白花蛇舌草提取物对肝癌细胞 JNK/p38MARK通路及细胞学行为的影响 |
| Effects of hedyotis diffusa extract on JNK/p38MARK pathway and cytological behavior of hepatoma cells |
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| DOI：10.3969/j.issn.1009-6469.2022.08.003 |
| 中文关键词: 白花蛇舌草提取物 肝肿瘤 c-Jun氨基末端激酶 /p38丝裂原活化蛋白激酶通路 QGY细胞株 增殖 凋亡 、P， |
| 英文关键词: Hedyotis diffusa extract Liver neoplasms C-Jun N-terminal kinase/p38 mitogen-activated protein kinase pathway QGY cell line Proliferation Apoptosis |
| 基金项目:国家自然科学基金( 81373513)； 2018年国家中医药管理局区域中医(肝病)诊疗中心培育单位建设项目［国中医药办医政函( 2017)39号］ |
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| 中文摘要: |
| 目的研究白花蛇舌草提取物( HDE)对肝癌 QGY细胞增殖、凋亡的影响，并探讨其抗肿瘤的可能作用机制。方法体外培养肝癌 QGY细胞，分为对照组: RPMI-1640培养基培养；阳性对照组:全反式维甲酸( AT-RA)(5 μmol/L)；白花蛇舌草提取物( HDE)低、中、高剂量组:分别给予 20、40、80 g/L HDE。四甲基偶氮唑盐比色法( MTT)检测细胞增殖能力，采用 Hoechst33258荧光染色以及流式 AnnexinV-FITC/PI双染法检测细胞凋亡率；通过蛋白质印迹法( Western blotting)检测增殖相关蛋白增殖细胞核抗原( PCNA)、凋亡相关蛋白 B淋巴细胞瘤基因 -2(Bcl-2)、 Bcl-2相关 X蛋白基因( Bax)、半胱氨酰天冬氨酸特异性蛋白酶 3(caspase3)及 JNK/p38MARK通路相关蛋白水平。结果 24、48 h时 QGY细胞增殖抑制率，与对照组［( 16.56± |
| 英文摘要: |
| Objective To study the effects of hedyotis diffusa extract (HDE) on the proliferation and apoptosis of hepatoma QGYcells, and to explore the possible mechanism of its anti-tumor effect.Methods The QGY cells were cultured in vitro and divided into control group: cultured in RPMI-1640 culture medium; positive control group: all trans retinoic acid (AT-RA) (5 μmol/L); low, mediumand high dose groups of Hedyotis diffusa extract (HDE): 20, 40 and 80 g/L HDE respectively. MTT method was used to detect cell pro-liferation, Hoechst33258 fluorescence staining and flow Annexin V-FITC/PI double staining were used to detect the apoptosis rate; in addition, the levels of proliferating cell nuclear antigen (PCNA), B-lymphoma gene-2 (Bcl-2), Bcl-2 related X protein gene (Bax), cas- pase-3 and JNK/p38MARK pathway related proteins were detected by Western blotting.Results Compared with those in the controlgroup[(16.56±3.15)%,(19.27±3.33)%] at the same time point, the inhibition rate of QGY cell proliferation in 20, 40, 80 g/L HDE groups[24 h(33.37±11.36)%,(47.57±13.62)%,(59.37±16.95)%,48 h(36.56±10.03)%,(50.59±13.87)%,(63.61±16.99)%] and positive controlgroup[(60.43±17.09)%,(64.63±17.15)%] at 24, 48 h increased significantly (P<0.05). Compared with those in the control group, the apoptosis rate, Bax and caspase-3 protein of QGY cells after treatment with HDE with concentration of 20, 40 and 80 g/L increased sig-nificantly (P < 0.05), the expressions of PCNA, Bcl-2 protein, p-JNK/JNK, p-p38/p38 decreased (P<0.05), and all of them were concen- tration dependent, while there was no significant difference in apoptosis rate, Bax, Caspase-3, PCNA, Bcl-2 protein, p-JNK/JNK, p-p38/ p38 expressions between the 80 g/L HDE group and the positive control group (P>0.05).Conclusion HDE can inhibit the prolifera- tion of QGY cells of liver cancer and promote the apoptosis of QGY cells, which may play an anti-tumor role by inhibiting the activation of JNK/p38MARK pathway. |
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