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黄芩苷调控自噬在癌症中的保护作用。

The protective role of baicalin regulation of autophagy in cancers.

作者信息

Zhang Qi, Guo Shiyun, Ge Hangwei, Wang Honggang

机构信息

Henan International Joint Laboratory for Nuclear Protein Regulation, School of Basic Medical Sciences, Henan University, Kaifeng, 475004 Henan China.

出版信息

Cytotechnology. 2025 Feb;77(1):33. doi: 10.1007/s10616-024-00689-0. Epub 2025 Jan 3.

DOI:10.1007/s10616-024-00689-0
PMID:39760060
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11699138/
Abstract

Autophagy is a conservative process of self degradation, in which abnormal organelles, proteins and other macromolecules are encapsulated and transferred to lysosomes for subsequent degradation. It maintains the intracellular balance, and responds to cellular conditions such as hunger or stress. To date, there are mainly three types of autophagy: macroautophagy, microautophagy and chaperone-mediated autophagy. Autophagy plays a key role in regulating multiple physiological and pathological processes, such as cell metabolism, development, energy homeostasis, cell death and hunger adaptation, and so on. Increasing evidence indicates that autophagy dysfunction participates in many kinds of cancers, such as liver cancer, pancreatic cancer, prostate cancer, and so on. However, the relevant mechanisms are not yet fully understood. Baicalin is a natural flavonoid compound extracted from the traditional Chinese medicine . The research has shown that after oral or intravenous administration of baicalin, it is delivered to various organs through the systemic circulation, with the highest volume in the kidneys and lungs. More and more evidence suggests that baicalin has antioxidant, anticancer, anti-inflammatory, anti-apoptotic, immunomodulatory and antiviral effects. Therefore, baicalin plays an important role in various diseases, such as cancers, lung diseases, liver diseases, cardiovascular diseases, ans so on. However, the relevant mechanisms have not yet been fully clear. Recently, increasing evidence indicates that baicalin participates in different cancer by regulating autophagy. Herein, we reviewed the current knowledge about the role and mechanism of baicalin regulation of autophagy in multiple types of cancers to lay the theoretical foundation for future related researches.

摘要

自噬是一种保守的自我降解过程,在此过程中,异常的细胞器、蛋白质和其他大分子被包裹并转移至溶酶体以便随后进行降解。它维持细胞内平衡,并对饥饿或应激等细胞状况作出反应。迄今为止,自噬主要有三种类型:巨自噬、微自噬和伴侣介导的自噬。自噬在调节多种生理和病理过程中起关键作用,如细胞代谢、发育、能量稳态、细胞死亡和饥饿适应等。越来越多的证据表明,自噬功能障碍参与多种癌症,如肝癌、胰腺癌、前列腺癌等。然而,相关机制尚未完全明确。黄芩苷是从中药中提取的一种天然黄酮类化合物。研究表明,口服或静脉注射黄芩苷后,它通过体循环输送到各个器官,在肾脏和肺中的含量最高。越来越多的证据表明,黄芩苷具有抗氧化、抗癌、抗炎、抗凋亡、免疫调节和抗病毒作用。因此,黄芩苷在各种疾病中发挥重要作用,如癌症、肺部疾病、肝脏疾病、心血管疾病等。然而,相关机制尚未完全清楚。最近,越来越多的证据表明,黄芩苷通过调节自噬参与不同类型的癌症。在此,我们综述了目前关于黄芩苷在多种癌症中调节自噬的作用和机制的认识,为未来相关研究奠定理论基础。

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本文引用的文献

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Baicalin Induces Gastric Cancer Cell Pyroptosis through the NF-κB-NLRP3 Signaling Axis.黄芩苷通过NF-κB-NLRP3信号轴诱导胃癌细胞焦亡
J Cancer. 2024 Jan 1;15(2):494-507. doi: 10.7150/jca.89986. eCollection 2024.
2
Baicalin and baicalein in modulating tumor microenvironment for cancer treatment: A comprehensive review with future perspectives.黄芩苷和黄芩素通过调节肿瘤微环境治疗癌症:综述及未来展望
Pharmacol Res. 2024 Jan;199:107032. doi: 10.1016/j.phrs.2023.107032. Epub 2023 Dec 5.
3
Curcumin in vitro Neuroprotective Effects Are Mediated by p62/keap-1/Nrf2 and PI3K/AKT Signaling Pathway and Autophagy Inhibition.姜黄素的体外神经保护作用由p62/keap-1/Nrf2和PI3K/AKT信号通路以及自噬抑制介导。
Physiol Res. 2023 Aug 31;72(4):497-510. doi: 10.33549/physiolres.935054.
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STING signalling is terminated through ESCRT-dependent microautophagy of vesicles originating from recycling endosomes.STING 信号通过起源于再循环内体的囊泡的 ESCRT 依赖性微自噬来终止。
Nat Cell Biol. 2023 Mar;25(3):453-466. doi: 10.1038/s41556-023-01098-9. Epub 2023 Mar 13.
5
Baicalin Blocks Colon Cancer Cell Cycle and Inhibits Cell Proliferation through miR-139-3p Upregulation by Targeting CDK16.黄芩苷通过靶向CDK16上调miR-139-3p来阻断结肠癌细胞周期并抑制细胞增殖。
Am J Chin Med. 2023;51(1):189-203. doi: 10.1142/S0192415X23500118. Epub 2023 Jan 4.
6
Macroautophagy in quiescent and senescent cells: a pathway to longevity?静止期和衰老期细胞中的巨自噬:通往长寿的途径?
Trends Cell Biol. 2023 Jun;33(6):495-504. doi: 10.1016/j.tcb.2022.10.004. Epub 2022 Nov 20.
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