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重楼皂苷VI通过活性氧介导的JNK和P38激活诱导胶质瘤细胞凋亡和自噬

Polyphyllin VI Induces Apoptosis and Autophagy via Reactive Oxygen Species Mediated JNK and P38 Activation in Glioma.

作者信息

Liu Wei, Chai Yi, Hu Libo, Wang Junhua, Pan Xin, Yuan Hongyu, Zhao Zitong, Song Yongmei, Zhang Yuqi

机构信息

School of Clinical Medicine, Tsinghua University, Beijing 10084, People's Republic of China.

Department of Neurosurgery, Yuquan Hospital, School of Clinical Medicine, Tsinghua University, Beijing 100040, People's Republic of China.

出版信息

Onco Targets Ther. 2020 Mar 13;13:2275-2288. doi: 10.2147/OTT.S243953. eCollection 2020.

DOI:10.2147/OTT.S243953
PMID:32214827
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7078907/
Abstract

BACKGROUND

Polyphyllin VI (PPVI), a bioactive component derived from a traditional Chinese herb , exhibits potential antitumor activity against hepatocellular carcinoma, as well as breast and lung cancers. However, its effect on glioma remains unknown.

METHODS

Five glioma cell lines (U251, U343, LN229, U87 and HEB) and an animal model were employed in the study. Anti-proliferation effects of PPVI were first determined using CCK-8 cell proliferation and clone formation assays, then reactive oxygen species (ROS), cell cycle progression and apoptosis effects measured by flow cytometry. The effect of PPVI on protein expression was quantified by Western blot analysis.

RESULTS

Data showed that PPVI inhibited the proliferation of glioma cell lines by modulating the G2/M phase. Additionally, incubation of cells with PPVI promoted apoptosis, autophagy, increased accumulation of ROS and activated ROS-modulated JNK and p38 pathways. On the other hand, N-acetyl cysteine, a ROS inhibitor, attenuated PPVI-triggered effects. Furthermore, JNK and p38 inhibitors ameliorated PPVI-triggered autophagy and apoptosis in glioma cells. In vivo assays showed that PPVI inhibited tumor growth of U87 cell line in nude mice.

CONCLUSION

Overall, these data suggested that PPVI might be an effective therapeutic agent for glioma.

摘要

背景

重楼皂苷VI（PPVI）是一种源自传统中药的生物活性成分，对肝细胞癌以及乳腺癌和肺癌具有潜在的抗肿瘤活性。然而，其对胶质瘤的作用尚不清楚。

方法

本研究采用了五种胶质瘤细胞系（U251、U343、LN229、U87和HEB）和一个动物模型。首先使用CCK-8细胞增殖和克隆形成试验确定PPVI的抗增殖作用，然后通过流式细胞术测量活性氧（ROS）、细胞周期进程和凋亡效应。通过蛋白质印迹分析定量PPVI对蛋白质表达的影响。

结果

数据显示，PPVI通过调节G2/M期抑制胶质瘤细胞系的增殖。此外，用PPVI处理细胞可促进凋亡、自噬，增加ROS的积累并激活ROS调节的JNK和p38通路。另一方面，ROS抑制剂N-乙酰半胱氨酸减弱了PPVI触发的效应。此外，JNK和p38抑制剂改善了PPVI触发的胶质瘤细胞自噬和凋亡。体内试验表明，PPVI抑制了裸鼠中U87细胞系的肿瘤生长。

结论

总体而言，这些数据表明PPVI可能是一种有效的胶质瘤治疗药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f528/7078907/4beb98bd616a/OTT-13-2275-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f528/7078907/0f90608a4d1b/OTT-13-2275-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f528/7078907/4beb98bd616a/OTT-13-2275-g0009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f528/7078907/0f90608a4d1b/OTT-13-2275-g0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/f528/7078907/66ddf45f83a7/OTT-13-2275-g0005.jpg
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