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中药有效成分逆转肝癌顺铂耐药机制的研究进展 被引量:2

Mechanism of effective components in traditional Chinese medicine against cisplatin-induced resistance of liver cancer
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摘要 肝癌是最常见的恶性肿瘤之一,也是全球癌症相关死亡的主要原因。顺铂是临床上治疗肝癌的一线化疗药物,然而不良反应和耐药性是顺铂治疗肝癌的两大挑战,因此一些天然产物作为潜在的抗癌药物和增敏剂引起了广大学者的密切关注。中药有效成分联合顺铂可发挥协同增效、降低化疗不良反应等作用来更好地抗肝癌。从逆转细胞凋亡受阻、调控细胞自噬、降低化疗药物浓度、诱导DNA损伤和抑制上皮–间充质转化5个方面综述中药有效成分逆转肝癌顺铂耐药的机制,以期为未来减轻临床肝癌顺铂耐药、提高肝癌患者的生存质量和治疗效果提供参考。 Liver cancer is one of the most common malignancies and is the leading cause of cancer-related death worldwide.Cisplatin is a first-line chemotherapy drug for the treatment of liver cancer in clinical practice.However,adverse reactions and drug resistance are the two major challenges of cisplatin in treatment of liver cancer.Therefore,some natural products as potential anticancer drugs and sensitizers have attracted close attention from scholars.The combination of effective ingredients of traditional Chinese medicine and cisplatin can better resist liver cancer by exerting synergistic effects and reducing chemotherapy adverse reactions.This article reviews the mechanisms of effective components in traditional Chinese medicine against cisplatin-induced resistance of liver cancer from five aspects:reversing cell apoptosis obstruction,regulating cell autophagy,reducing drug concentration,inducing DNA damage,and inhibiting epithelial mesenchymal transition,to provide reference for reducing cisplatin-induced resistance against liver cancer in clinics,improving the quality of life and treatment effectiveness of liver cancer patients in the future.
作者 徐瑞雪 王宇 XU Ruixue;WANG Yu(School of Basic Medicine,Shaanxi University of Chinese Medicine,Xianyang 712046,China;Medical Research Experimental Center,Shaanxi University of Chinese Medicine,Xianyang 712046,China)
出处 《现代药物与临床》 CAS 2024年第1期257-262,共6页 Drugs & Clinic
基金 国家自然科学基金资助项目(81402344) 陕西省自然科学基础研究计划项目(2020JM-595,2023-JC-YB-745)。
关键词 中药 有效成分 顺铂 肝癌 耐药 凋亡 细胞自噬 药物浓度 DNA损伤 上皮-间充质转化 traditional Chinese medicine effective component cisplatin liver cancer resistance apoptosis cell autophagy drug concentration DNA damage epithelial mesenchymal transition
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