甲状腺巴巴丁B通过通过多种途径诱导细胞循环停止和细胞亡来表现出抗乳腺癌活性
Chong Niu1, Ruo-Tong Li2, Xiao-Shan Hao1
1School of Pharmacy (Institute of Pharmaceutical Research), Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, Shandong, People's Republic of China.
Phytotherapy research : PTR
|June 30, 2025
概括
来自S. barbata的Scutebarbatine B (SBT-B) 显示出作为乳腺癌治疗的潜力. 它抑制癌细胞增殖,诱导DNA损伤和亡,并激活关键信号通路.
科学领域:
- 药理学和毒理学 药理学和毒理学
- 在瘤学瘤学.
- 自然产品化学 自然产品化学
背景情况:
- 乳腺癌仍然是女性死亡的主要原因,需要新的治疗策略.
- 从自然来源中识别有效的抗癌化合物对于改善患者生存率至关重要.
- 斯库特拉里亚巴巴塔D.唐 (S. barbata) 是一种具有潜在药用功能的传统草药.
研究的目的:
- 为了研究Scutebarbatine B (SBT-B) 的抗癌作用,S. barbata的二类化物,对乳腺癌.
- 阐明SBT-B在体外和体内对抗乳腺癌活性的潜在分子机制.
主要方法:
- 在体外测试包括细胞活力,EDU,免疫光,流细胞计,TUNEL染色,西部斑点和ROS检测 (DCFH-DA,DHE).
- 在体内有效性使用老鼠异种移植模型进行了评估.
- 分析了关键的分子通路 (pRB/E2F1,Akt/mTOR,IRE1/JNK) 和亡标记物 (caspase-8, -9,PARP) 的情况.
主要成果:
- SBT-B抑制了乳腺癌细胞的增殖,并诱导了G2/M阶段的停止,降低了循环素和Cdc2.
- SBT-B通过增加酶和PARP裂变以及提高细胞内活性氧物种 (ROS) 生成来触发亡.
- 在体内,SBT-B抑制了瘤生长,抑制了pRB/E2F1和Akt/mTOR通路,并激活了IRE1/JNK通路.
结论:
- 斯库特巴巴丁B (SBT-B) 通过诱导DNA损伤,细胞循环停止和亡,显示出对乳腺癌的显著抗癌活性.
- 产生ROS,抑制瘤信号传递和激活IRE1/JNK通路是SBT-B有效性的关键机制.
- SBT-B显示出作为治疗人类乳腺癌的潜在替代治疗候选人的承诺.
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