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Preparation of Naringenin Solution for In Vivo Application
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纳灵宁通过ROS介导的JAK-2/STAT-3信号通路诱导HepG2细胞亡
Ming Zhang1, Jianmei Lai2, Qianlong Wu2
1Department of Interventional Radiology and Vascular Anomalies, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou 510120, China.
Molecules (Basel, Switzerland)
|June 10, 2023
概括
类化合物纳灵宁通过触发氧化应激和抑制关键信号通路,有效地诱导肝癌 (肝癌) 细胞的亡. 这表明纳林根宁.
科学领域:
- 肝细胞癌研究 肝细胞癌研究
- 癌症生物学 癌症生物学
- 自然产品药理学 自然产品药理学
背景情况:
- 肝细胞癌 (HCC) 是一种流行癌症,治疗选择有限.
- 类植物中的一种黄类化合物纳灵宁 (Naringenin) 显示出潜在的抗癌作用,但其在HCC中的机制尚不清楚.
- 了解纳林根因对HCC细胞中氧化应激和亡的影响至关重要.
研究的目的:
- 为了研究在HepG2肝癌细胞中纳灵的细胞毒性和抗癌机制.
- 为了阐明氧化应激在纳灵宁诱导的细胞死亡中的作用.
- 探索纳林根因对亡相关信号通路的影响.
主要方法:
- 治疗HepG2细胞时使用了纳灵宁.
- 通过流细胞计 (G1亚种群,酸暴露,线粒体潜力),DNA碎片化试验和酶激活 (酶-3,酶-9) 评估了亡.
- 分析了细胞内活性氧物种 (ROS) 水平和JAK-2/STAT-3信号通路活性.
主要成果:
- 纳灵宁诱导了HepG2细胞的显著亡,由增加的亚G1细胞数量,酸酶外化,线粒体功能障碍和DNA碎片化所证明.
- 纳灵宁治疗导致了-3和-9的激活.
- 纳灵宁通过增加细胞内ROS和抑制JAK-2/STAT-3信号通路来增强细胞毒性,进一步促进细胞亡.
结论:
- 纳灵宁通过多种机制有效地诱导肝癌细胞的亡,包括氧化应激诱导和JAK-2/STAT-3通路抑制.
- 纳灵宁对HepG2细胞表现出显著的细胞毒性作用.
- 纳灵宁作为肝癌治疗的潜在治疗剂具有前途.
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