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远志酮 D 通过调控 MAPK 通路诱导结肠癌细胞凋亡并促进自噬

Platycodin D induces apoptosis via regulating MAPK pathway and promotes autophagy in colon cancer cell.

机构信息

Department of Companion and Laboratory Animal Science, Kongju National University, Yesan 32439, Republic of Korea.

Department of Companion and Laboratory Animal Science, Kongju National University, Yesan 32439, Republic of Korea; Research Institute for Natural Products, Kongju National University, Yesan, Republic of Korea.

出版信息

Biomed Pharmacother. 2024 Mar;172:116216. doi: 10.1016/j.biopha.2024.116216. Epub 2024 Jan 31.

Abstract

Platycodin D (PD) is the main component of triterpene saponins found in Platycodi radix. In this study, we observed a decrease in cell viability, an increase in apoptotic bodies, and an increase in the rate of apoptosis. Also, we observed an increase in cleaved PARP and Bax, a decrease in Bcl-2, and p-ERK, and an increase in p-p38 and p-JNK. Furthermore, a change in cell viability and the expression of p-p38, Bax, and Bcl-2 using the p38 inhibitor revealed a decrease in p-p38 and Bax and an increase in Bcl-2 in the inhibitor treatment group. In addition, we observed an increase in vacuole formation through morphological changes and an increase in acidic vesicular organelles (AVOs). We also observed an increase in the expression of beclin 1, LC 3-I, and -II. There was no significant decrease in cell viability in the group treated with 3-MA, but a decrease in cell viability was noted in the group treated with HCQ. HCQ treatment resulted in an increase in Bax and a decrease in Bcl-2. These findings reveal that in HT-29 colon cancer cells, PD induces apoptosis through the MAPK pathway, thereby exerting anticancer effects. Moreover, autophagy caused by PD inhibits apoptosis by protecting the cells.

摘要

远志皂苷 D (PD) 是桔梗中的三萜皂苷的主要成分。在本研究中,我们观察到细胞活力下降,凋亡小体增加,细胞凋亡率增加。此外,还观察到 cleaved PARP 和 Bax 增加,Bcl-2 和 p-ERK 减少,p-p38 和 p-JNK 增加。进一步用 p38 抑制剂观察细胞活力变化和 p-p38、Bax 和 Bcl-2 的表达,发现抑制剂处理组中 p-p38 和 Bax 减少,Bcl-2 增加。此外,通过形态变化观察到空泡形成增加和酸性囊泡细胞器 (AVOs) 增加。还观察到 beclin 1、LC 3-I 和 -II 的表达增加。3-MA 处理组细胞活力无明显下降,但 HCQ 处理组细胞活力下降。HCQ 处理导致 Bax 增加,Bcl-2 减少。这些发现表明,在 HT-29 结肠癌细胞中,PD 通过 MAPK 通路诱导细胞凋亡,从而发挥抗癌作用。此外,PD 引起的自噬通过保护细胞来抑制细胞凋亡。

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