CLC number:
On-line Access: 2022-08-12
Received: 2022-01-22
Revision Accepted: 2022-04-27
Crosschecked: 2022-08-12
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Citations: Bibtex RefMan EndNote GB/T7714
Yang CHEN, Qian LI, Sisi REN, Ting CHEN, Bingtao ZHAI, Jiangxue CHENG, Xiaoyan SHI, Liang SONG, Yu FAN, Dongyan GUO. Investigation and experimental validation of curcumin-related mechanisms against hepatocellular carcinoma based on network pharmacology[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2200038 @article{title="Investigation and experimental validation of curcumin-related mechanisms against hepatocellular carcinoma based on network pharmacology", %0 Journal Article TY - JOUR
基于网络药理学的姜黄素防治肝癌分子机制的探究与验证1陕西中医药大学基础医学院,陕西咸阳,712046 2陕西中医药大学药学院,陕西咸阳,712046 3陕西中医药大学医学科研实验中心,陕西咸阳,712046 4陕西省中医体质与疾病防治研究重点实验室,陕西咸阳,712046 目的:运用网络药理学和体外细胞实验探究姜黄素防治肝癌的分子机制。 创新点:运用网络药理学预测姜黄素作用与肝癌防治间的相关性及作用靶点。以此为基础,探索姜黄素是否通过能量代谢感受器AMPK诱导AMPK/ULK1自噬通路并触发自噬性凋亡减轻肝癌;并对姜黄素诱导肝癌细胞凋亡时,是否存在p53/DRAM凋亡促自噬通路进行验证;最后研究在姜黄素治疗肝癌中,细胞凋亡和细胞自噬是否通过DRAM和p62相互转移。 方法:从多个数据库收集姜黄素作用和肝癌治疗潜在靶点,利用DAVID平台将交集靶点进行GO和KEGG分析,预测姜黄素防治肝癌的相关信号通路。结合预测结果,采用MTT法检测姜黄素对HepG2和LO2细胞活力的影响;运用流式细胞术和透射电镜检测姜黄素处理后,HepG2细胞的凋亡和自噬情况;并经western blot和real-time PCR验证p53凋亡及AMPK自噬通路在姜黄素治疗肝癌中的作用。最后,通过p53抑制剂pifithrin-α和AMPK抑制剂GSK690693的使用进一步探索姜黄素治疗肝癌潜在的分子机制。 结论:姜黄素可通过p53凋亡和AMPK/ULK1自噬途径治疗肝癌,其中自噬和凋亡可能通过DRAM和p62相互转化。 关键词组: Darkslateblue:Affiliate; Royal Blue:Author; Turquoise:Article
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