首页|从肿瘤细胞黏附异常探讨慢性应激加剧肿瘤转移的中医药防治思路

从肿瘤细胞黏附异常探讨慢性应激加剧肿瘤转移的中医药防治思路

Exploring the Ideas of Traditional Chinese Medicine in the Prevention and Treatment of Tumour Metastasis Exacerbated by Chronic Stress:from the Perspective of Abnormal Tumour Cell Adhesion

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肿瘤细胞黏附异常是肿瘤转移的关键步骤,其中肿瘤细胞的同源黏附减弱、异源黏附增强是导致肿瘤转移的重要原因.慢性应激可激活交感神经系统联动调控肿瘤细胞的同源与异源黏附而加剧肿瘤转移.结合中医学和西医学对肿瘤转移的认识,认为中医理论中"气机郁滞、癌毒传舍"病机与慢性应激触发的肿瘤细胞黏附异常具有高度关联性,气机郁滞与慢性应激及其激活的交感神经系统关系密切,癌毒传舍则从中医学角度阐释了肿瘤细胞黏附异常而致肿瘤转移的机制.调气解毒方药可通过调控"交感神经系统—肿瘤细胞黏附"的关键环节达到改善慢性应激并抑制肿瘤转移的目的.
Abnormal tumour cell adhesion is a key step in tumour metastasis,in which weakened homologous and enhanced heterologous adhesion of tumour cells is an important cause of tumour metastasis.Chronic stress can activate the sympathetic nervous system to link and regulate the homologous and heterologous adhesion of tumour cells and exacerbate tumour metastasis.Combining the understanding of traditional Chinese medicine(TCM)and Western medicine on tumour metastasis,it is believed that the mechanism of"qi constraint and stagnation,tumor toxin trans-mission and retention"in TCM theory is highly related to the abnormal adhesion of tumour cells triggered by chronic stress.Qi constraint and stagnation is closely related to chronic stress and its activation of the sympathetic nervous system,and transmission and retention of tumor toxin explained the mechanism of tumour metastasis due to abnormal adhesion of tumour cells from the perspective of TCM.By regulating the key link of sympathetic nervous system-tumour cell adhesion,application of the formulas of regulating qi and resolving toxin can improve chronic stress and inhibit tumour metastasis.

tumour metastasischronic stresstumor cell adhesionconstraint and stagnation of the qitumor toxin

赵凡、尹刚、谭峰、温芳、瞿融、唐德才

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南京中医药大学中医学院,江苏省南京市栖霞区仙林大道138号,210023

肿瘤转移 慢性应激 肿瘤细胞黏附 气机郁滞 癌毒

国家自然科学基金国家中医药局高水平中医药重点学科建设项目江苏省中医药局省中医药科技发展计划南京中医药大学国家自然科学基金青年科学基金经费配套项目

82204641国中医药人教函[2023]85号QN202104XPT82204641

2024

10.13288/j.11-2166/r.2024.09.005

中医杂志
中华中医药学会 中国中医科学院

中医杂志

CSTPCD北大核心
影响因子：1.464
ISSN：1001-1668
年,卷(期)：2024.65(9)
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