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基于网络药理的分析和体外实验验证显示,酸通过PI3K/AKT/HSP90途径在HepG2细胞中诱导细胞亡

Jingyang Lu^1,2, Yue Qiu^1,2, Facheng Bai³

¹Pharmacy Department, The First Affiliated Hospital of Guangxi Medical University, Nanning, Guangxi, China.

Chemical biology & drug design

|January 16, 2026

概括

酸 (TA) 显示出对抗肝癌 (HCC) 的承诺. 它通过调节PI3K/AKT/HSP90通路来抑制癌细胞生长并触发细胞亡,这是体外研究证实的.

科学领域:

药理学药理学是指药理学的学科.
生物信息学是一种生物信息学.
在瘤学瘤学.

背景情况:

肝细胞癌 (HCC) 是一个主要的全球健康问题,治疗选择有限.
酸 (TA) 已显示出对HCC的潜在治疗作用.
了解TA的机制对于开发新的抗HCC策略至关重要.

研究的目的:

为了研究门酸 (TA) 的抗HCC作用.
通过多组学方法阐明TA对HCC的作用的潜在分子机制.
通过体外实验验验验证发现.

主要方法:

网络药理学以确定TA的目标和途径.
生物信息学分析包括基因本体学 (GO) 和基因和基因组的京都百科全书 (KEGG) 路径丰富.
分子对接和分子动力学模拟用于结合亲和力和稳定性.
在HepG2细胞中进行体外测试 (CCK-8,流细胞测量,西式涂抹).

主要成果:

网络药理学确定了细胞亡和PI3K/AKT/HSP90通路作为TA抗HCC作用的关键调解者.
分子模拟证实了TA及其标蛋白之间的稳定相互作用.
试验室实验表明TA有抑制HepG2细胞增殖和诱导亡的能力.
西部涂抹显示TA调节了Bax,Bcl-2,PI3K,AKT和HSP90的表达.

结论:

酸通过抑制细胞增殖和诱导亡,表现出显著的抗HCC特性.
PI3K/AKT/HSP90信号通路是TA抗癌活性的一个关键目标.
TA代表了肝细胞癌的潜在治疗剂.

关键词:

在PI3K/AKT/HSP90信号通路中.门酸是一种门酸.灭症 (apoptosis) 是一种死亡的过程.肝细胞癌是肝细胞癌.网络药理学网络药理学

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