普拉提科丁D通过调节MAPK通路诱导亡,并促进结肠癌细胞的自
So-Hee Han1, Jae-Han Lee1, Joong-Seok Woo1
1Department of Companion and Laboratory Animal Science, Kongju National University, Yesan 32439, Republic of Korea.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
|January 31, 2024
概括
来自Platycodi radix的Platycodin D通过MAPK通路诱导结肠癌细胞的亡. 然而,由Platycodin D触发的自异常地保护细胞,抑制抗癌效应.
科学领域:
- 药理学 药理学是指药理学的学科.
- 分子生物学分子生物学
- 癌症研究 癌症研究
背景情况:
- 普拉蒂科迪根是一种传统的草药.
- 普拉提科丁D (PD) 是一个关键的三三香成分.
- 结肠癌仍然是一个重大的全球健康挑战.
研究的目的:
- 为了研究Platycodin D (PD) 对HT-29结肠癌细胞的抗癌作用.
- 阐明PD的作用背后的分子机制,重点关注亡和自.
- 确定MAPK信号通路在PD诱导的细胞毒性中的作用.
主要方法:
- 细胞活力测试 (MTT).
- 亡评估 (亡体,裂开的PARP,巴克斯,BCL-2表达).
- 西方涂抹用于信号蛋白 (p-ERK,p-p38,p-JNK,贝克林1,LC3-I/II).
- 自评估 (真空球形成,酸性囊泡器官 - AVOs).
- 药理上抑制p38 MAPK和自 (3-MA,HCQ).
主要成果:
- PD显著降低HT-29细胞活力,并诱导了亡.
- 与亡相关的PD调节蛋白质 (增加裂解PARP,Bax;降低Bcl-2).
- PD激活了MAPK通路 (增加了p-p38,p-JNK;减少了p-ERK).
- 导致PD的自标志物 (空腔形成,AVO,贝克林1,LC3-I/II).
- p38 MAPK抑制减少了PD对亡的影响.
- 自抑制 (HCQ) 增强了PD的细胞毒性作用,而3-MA对生存能力没有显著影响.
结论:
- 普拉提科丁D通过MAPK信号通路诱导亡,对HT-29结肠癌细胞表现出抗癌性质.
- PD还会触发自,这似乎是作为一种保护机制,部分抵消其亡效应.
- 向亡和自途径可能会增强Platycodin D在结肠癌治疗中的治疗潜力.
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