胃复春对胃底腺息肉有促进铁下垂的治疗作用。

L I Yue, Deng Jinyan, P I Shanshan, Zhang Yingjuan, Zhao Dan, Guo Yi, Y E Yong'an, Zao Xiaobin, D U Hongbo
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引用次数: 0

摘要

目的:观察中药胃复春对胃底腺息肉的治疗作用。方法:用患者源性标本构建FGPs类器官。采用明场成像技术检测FGPs类器官的形态和大小。通过多个开源数据库和中药或复方研究,筛选WFC的有效成分和相应的潜在靶点。通过蛋白-蛋白相互作用网络鉴定核心基因。对核心基因进行京都基因与基因组百科全书(KEGG)和基因本体(GO)富集分析。通过FerrDb数据库分析主要部件与核心目标之间的相互作用。采用实时荧光定量聚合酶链反应(qRT-PCR)检测核心靶点的表达。结果:经WFC处理后,fgp类器官的数量和大小均明显减少。共鉴定出WFC治疗fgp的活性成分29个,候选靶点162个,其中与铁下垂相关的靶点37个。槲皮素、青花花素B、青花花素U、青花花素O、橙皮素、青花花素A、Angustifolin、青花花素M、邻苯二甲酸二辛酯和β -谷甾醇为主要活性成分。SRC原癌基因、非受体酪氨酸激酶、信号转导和转录激活因子3、磷脂酰肌醇-4,5-二磷酸3-激酶催化亚基α、磷脂酰肌醇-4,5-二磷酸3-激酶催化亚基β、磷脂酰肌醇-3-激酶调控亚基1和AKT丝氨酸/苏氨酸激酶1被确定为主要靶点。KEGG通路与癌变、细胞增殖和代谢以及氧化应激有关。WFC可促进fgp类器官的死亡,并可通过Erastin抑制剂逆转。qRT-PCR结果显示,WFC处理可调节溶质载体家族7成员11、酰基辅酶a合成酶长链家族成员4、花生四烯酸15-脂氧合酶b型mRNA表达水平。结论:WFC可能通过诱导fgp细胞铁下垂发挥其治疗作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Weifuchun ( ) exerts therapeutic effects on gastric fundic gland polyps by promoting ferroptosis.

Objective: To investigate the therapeutic effects of Chinese medicine Weifuchun (WFC, ) on gastric fundic gland polyps (FGPs).

Methods: FGPs organoids were constructed with patients-derived samples. The morphology and size of FGPs organoids were detected using bright-field imaging. Effective components and corresponding potential targets of WFC were screened using multiple open-source databases and research on Traditional Chinese Medicine or compound formulas. Core genes were identified through protein-protein interaction networks. Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) enrichment analyses of the core genes were conducted. The interactions between main components and core targets were analyzed through the FerrDb database. The expressions of core targets were detected by quantitative real-time polymerase chain reaction (qRT-PCR).

Results: After WFC treatment, the number and size of FGPs organoids were significantly reduced. Twenty nine active drug components and 162 candidate targets of WFC for treating FGPs were identified, including 37 targets related to ferroptosis. Quercetin, Glaucocalyxin B, Melissoidesin U, Melissoidesin O, Hesperetin, Glaucocalyxin A, Angustifolin, Melissoidesin M, Di-n-octyl phthalate, and beta-sitosterol were identified as the main active compounds. SRC proto-oncogene, non-receptor tyrosine kinase, signal transducer and activator of transcription 3, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha, phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit beta, phosphoinositide-3-kinase regulatory subunit 1, and AKT serine/threonine kinase 1 were identified as the primary targets. KEGG pathways related to carcinogenesis, cell proliferation and metabolism, and oxidative stress. WFC promoted FGPs organoids' death and could be reversed by ferroptosis inhibitor of Erastin. The qRT-PCR results showed that WFC treatment could regulate the mRNA expression levels of solute carrier family 7 member 11, acyl-CoA synthetase long chain family member 4, and arachidonate 15-lipoxygenase, type B.

Conclusion: WFC may exert its therapeutic effects by inducing ferroptosis in FGPs cells.

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