共查询到18条相似文献,搜索用时 250 毫秒
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隐丹参酮(CTS)是从中草药丹参根茎中提取的单体成分,相对分子质量小,可透过血脑屏障,近年来通过体内外各种实验被证实对冠心病、动脉粥样硬化、关节炎、内分泌失衡、脑损伤和阿尔茨海默病等疾病具有药理活性。在抗肿瘤方面不仅可通过抑制细胞增殖、诱导肿瘤细胞凋亡、抑制肿瘤细胞转移侵袭和抗新生血管生成等机制而发挥抗肿瘤作用,同时还具有与部分化疗药物联合,增敏化疗疗效或逆转化疗耐药的作用。通过对CTS在各种肿瘤中的抗肿瘤药理活性与逆转肿瘤耐药进行综述,为其在临床研究中的应用提供参考。 相似文献
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化疗是目前治疗肿瘤主要手段之一,而在治疗过程中产生的多药耐药(multidrug resistance,MDR)现象却是造成化疗失败的主要因素。多药耐药是指肿瘤对一种抗肿瘤药物出现耐药的同时,对其他许多结构各异、作用机制不同的抗肿瘤药物亦产生交叉耐药现象。因此,研究MDR产生的机制、寻求有效的耐药逆转剂及逆转措施,克服MDR现象已成为国内外的研究热点。 相似文献
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甘草的主要成分甘草酸及其代谢产物甘草次酸具有诸多药理活性,包括传统的抗炎、免疫调节、抗肝损伤,及现今的研究热点抗病毒及抗肿瘤作用。笔者就10年来对甘草酸以及甘草次酸国外药理学进展、及其作用机制研究做一综述。 相似文献
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肿瘤多药耐药是肿瘤治疗过程中一个亟待解决的难题,其表现为肿瘤细胞对单一或多种化疗药物同时出现耐药性,从而导致治疗失败,与药物的化学结构和作用机制无关。将化疗药物与肿瘤多药耐药逆转剂联合应用是目前公认的治疗方案之一。黄酮类化合物由于其低毒、高效,具有多种药理作用等优点而受到广泛的关注。在肿瘤治疗期间,黄酮类化合物能通过抑制ABC转运体、诱导凋亡、调节氧化应激等作用逆转肿瘤多药耐药。归纳总结了黄酮类化合物逆转肿瘤多药耐药的主要机制、应用及其纳米剂型改造的进展,为进一步的临床研究提供参考。 相似文献
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肿瘤多药耐药(multidrug resistance,MDR)对肿瘤的药物治疗的疗效有严重的影响。多药耐药拥有十分复杂的发生发展的机制。通过讨论自噬与药物抗肿瘤时的相互影响,旨在阐明自噬与肿瘤细胞多药耐药的关系,为今后抗肿瘤药物治疗的临床应用提供新的思路。 相似文献
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肿瘤多药耐药(MDR)是导致肿瘤化疗失败的主要原因之一。肿瘤MDR的机制有多种,其中外排型转运体的过表达是导致MDR的主要机制,因此研究外排型转运体介导的肿瘤MDR机制和发现可以逆转肿瘤MDR的抑制剂成为国内外研究的热点。就目前研究的3种三磷酸腺苷结合盒转运体:P-糖蛋白、多药耐药相关蛋白、乳腺癌耐药蛋白介导的MDR及逆转MDR的机制进行综述,以期为提高肿瘤治疗疗效提供依据。 相似文献
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肿瘤多药耐药逆转剂的研究进展 总被引:16,自引:9,他引:16
肿瘤细胞产生的多药耐药(multidrugresistanceMDR)已成为当前影响肿瘤化学治疗疗效的主要障碍。尽管MDR产生机制复杂,但是由mdr1基因编码的P糖蛋白(PglycoproteinPgp)的过表达是产生MDR的主要原因。寻找低毒有效的MDR逆转剂是提高化疗疗效的一个重要方法,是化疗领域亟需解决的问题。 相似文献
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多药耐药基因与体外药敏检测在急性白血病中的临床意义 总被引:5,自引:0,他引:5
目的:研究急性白血病(AL)多药耐药-1(MDR1)基因表达与临床疗效的关系,提高对肿瘤细胞耐药情况预测的准确性。方法:采用逆转录敏-多聚酶链反应(RT-PCR)检测了30例AL患者骨髓中MDR1基因的表达,同时对每例均进行体外化疗药物敏感性(TMM)检测。结果:30例AL MDR1基因过度表达占40%,MTT检出耐药为30%(10/30),即有MDR1基因过量表达又显示耐药者27%(8/30); 相似文献
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Hongyu Yuan Xun Li Xianjun Qu Lirui Sun Wenfang Xu Wei Tang 《Medicinal chemistry research》2009,18(8):671-682
P-glycoprotein-mediated drug efflux from cells is believed to be an important mechanism in multidrug resistance (MDR) in cancer
chemotherapy. The identification and development of P-glycoprotein inhibitors with high potency and low cytotoxicity holds
great promise for overcoming MDR. A series of quinoxalinone derivatives were synthesized and evaluated primarily for their
antiproliferative effect and MDR reversal activity in in vitro assay systems. Biological assays demonstrated that the compounds
were, in general, endowed with good activity as P-glycoprotein inhibitors. Among them, compounds 10 and 16, which showed the highest MDR reversal activity without significant cytotoxicity, displayed potent P-glycoprotein inhibition
activities and may be worthy of further research as potential adjunctive agents for tumor chemotherapy. 相似文献
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Cyclooxygenase-2: potential role in regulation of drug efflux and multidrug resistance phenotype 总被引:19,自引:0,他引:19
Sorokin A 《Current pharmaceutical design》2004,10(6):647-657
Multidrug resistance (MDR) of cancer cells to cytostatic agents is the major obstacle for the succesfull chemotherapy. One of the causes of the development of cellular resistance to a wide variety of drugs is the elevated expression of membrane transporter proteins such as members of ATP binding cassette (ABC) protein superfamily. Expression of the ABC transporter MDR1, also termed P-glycoprotein (P-gp), seems to correlate with drug resistance of tumors to chemotherapy. Cyclooxygenase-2, an inducible isoform of enzyme, responsible for generation of prostaglandins from arachidonic acid, is constitutively expressed in a number of cancer cells. Anti-cancer potency of cyclooxygenase inhibitors is established, but the mechanism of Cox-2-dependent potentiation of tumor growth is a subject of intense discussion. Here we focus on the discussion of potential link between Cox-2 expression and development of multidrug resistance phenotype. Our observation, that enforced expression of Cox-2 causes enhancement in MDR1 expression and functional activity suggests the existence of causal link between Cox-2 activity and MDR1 expression. The use of Cox-2 inhibitors to decrease function of MDR1 may enhance accumulation of chemotherapy agents and decrease resistance of tumors to chemotherapeutic drugs. 相似文献
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《药学学报(英文版)》2023,13(3):982-997
Chemotherapy is one of the important methods to treat cancer, and the emergence of multidrug resistance (MDR) is one major cause for the failure of cancer chemotherapy. Almost all anti-tumor drugs develop drug resistance over a period of time of application in cancer patients, reducing their effects on killing cancer cells. Chemoresistance can lead to a rapid recurrence of cancers and ultimately patient death. MDR may be induced by multiple mechanisms, which are associated with a complex process of multiple genes, factors, pathways, and multiple steps, and today the MDR-associated mechanisms are largely unknown. In this paper, from the aspects of protein–protein interactions, alternative splicing (AS) in pre-mRNA, non-coding RNA (ncRNA) mediation, genome mutations, variance in cell functions, and influence from the tumor microenvironment, we summarize the molecular mechanisms associated with MDR in cancers. In the end, prospects for the exploration of antitumor drugs that can reverse MDR are briefly discussed from the angle of drug systems with improved targeting properties, biocompatibility, availability, and other advantages. 相似文献