首页> 美国卫生研究院文献>Oncotarget >Antrodia cinnamomea alleviates cisplatin-induced hepatotoxicity and enhances chemo-sensitivity of line-1 lung carcinoma xenografted in BALB/cByJ mice
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Antrodia cinnamomea alleviates cisplatin-induced hepatotoxicity and enhances chemo-sensitivity of line-1 lung carcinoma xenografted in BALB/cByJ mice

机译:牛樟芝可减轻顺铂诱导的肝毒性并增强BALB / cByJ小鼠异种移植的1线肺癌的化学敏感性

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摘要

Whereas cisplatin (cis-diamminedichloroplatinum II) is a first-line medicine to treat solid cancerous tumors, it often causes serious side effects. New medicines that have an equivalent or even better therapeutic effect but with free or less side effects than cisplatin are highly anticipated in cancer therapy. Recent reports revealed that Antrodia cinnamomea (AC) possesses hepatoprotective activity in addition to anticancer. In this study, we wanted to know whether AC enhances chemo-sensitivity of cisplatin and/or alleviates cisplatin-induced hepatotoxicity, as well as the underlying mechanisms thereof. Our results indicated that AC inhibited proliferation of line-1 lung carcinoma cells and rescued hepatic HepG2 cells from cisplatin-induced cell death in vitro. The fact is that AC and cisplatin synergized to constrain growth of line-1 lung carcinoma cells in BALB/cByJ mice. Quantitative real-time PCR further revealed that AC promoted expression of apoptosis-related genes, while it decreased expression of NF-κB and VEGF in tumor tissues. In liver, AC reduced cisplatin-induced liver dysfunctions, liver inflammation and hepatic apoptosis in addition to body weight restoration. In summary, AC is able to increase cisplatin efficacy by triggering expression of apoptosis-related genes in line-1 lung cancer cells as well as to protect liver from tissue damage by avoiding cisplatin-induced hepatic inflammation and cell death.
机译:顺铂(cis-diamminedichloroplatinum II)是治疗实体癌肿瘤的一线药物,但通常会引起严重的副作用。在癌症治疗中,人们高度期待具有与顺铂相当甚至更好的治疗效果但与顺铂相比具有更少或更少的副作用的新药。最近的报道显示,牛樟芝(AC)除具有抗癌作用外,还具有保肝活性。在这项研究中,我们想知道AC是否会增强顺铂的化学敏感性和/或减轻顺铂诱导的肝毒性,以及其潜在机制。我们的结果表明,AC抑制了1型肺癌细胞的增殖,并从顺铂诱导的细胞死亡中拯救了肝HepG2细胞。事实是,AC和顺铂协同作用以抑制BALB / cByJ小鼠中1系肺癌细胞的生长。实时定量PCR进一步揭示了AC促进了肿瘤组织中凋亡相关基因的表达,同时降低了NF-κB和VEGF的表达。在肝脏中,除体重恢复外,AC还减少了顺铂引起的肝功能障碍,肝脏炎症和肝细胞凋亡。总之,AC能够通过触发1型肺癌细胞中凋亡相关基因的表达来提高顺铂功效,并通过避免顺铂引起的肝炎和细胞死亡来保护肝脏免受组织损伤。

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