首页> 外文期刊>Food and Chemical Toxicology: An International Journal Published for the British Industrial Biological Research >Tanshinone IIA sodium sulfonate protects against cardiotoxicity induced by doxorubicin in vitro and in vivo.
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Tanshinone IIA sodium sulfonate protects against cardiotoxicity induced by doxorubicin in vitro and in vivo.

机译:丹参酮IIA磺酸钠可在体内和体外防御阿霉素引起的心脏毒性。

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摘要

Although doxorubicin (DXR) is an effective antineoplastic agent; the serious cardiotoxicity mediated by the production of reactive oxygen species has remained a considerable clinical problem. Our hypothesis is that tanshinone IIA sodium sulfonate (TSNIIA-SS), which holds significant affects on cardioprotection in clinic, protects against DXR-induced cardiotoxicity. In vitro investigation on H9c2 cell line, as well as in vivo study in animal model of DXR-induced chronic cardiomyopathy were performed. TSNIIA-SS significantly increased cell viability and ameliorated apoptosis of DXR-injured H9c2 cells using CCK-8 assay and Hoechst 33342 stain respectively. Furthermore, the cardio-protective effects of TSNIIA-SS were confirmed with decreasing ST-interval and QRS interval by electrocardiography (ECG); improving appearance of myocardium with haematoxylin and eosin (H&E) stain; increasing myocardial tensile strength using tension to rupture (TTR) assay and decreasing fibrosis through picric-sirius red staining comparing with those receiving DXR alone. These data have provided the considerable evidences that TSNIIA-SS is a protective agent against DXR-induced cardiac injury.
机译:尽管阿霉素(DXR)是有效的抗肿瘤药;由活性氧的产生介导的严重心脏毒性仍然是一个相当大的临床问题。我们的假设是丹参酮IIA磺酸钠(TSNIIA-SS)在临床上对心脏保护具有重要影响,可防止DXR诱导的心脏毒性。进行了H9c2细胞系的体外研究以及DXR诱发的慢性心肌病动物模型的体内研究。分别使用CCK-8分析和Hoechst 33342染色,TSNIIA-SS显着提高了DXR损伤的H9c2细胞的细胞活力并改善了其凋亡。此外,通过心电图(ECG)证实了STNIIA-SS的心脏保护作用具有减小的ST间隔和QRS间隔。用苏木精和曙红(H&E)染色改善心肌的外观;与仅接受DXR的患者相比,使用张力断裂(TTR)分析可提高心肌的抗张强度,并通过苦味-鼻窦红染色来减少纤维化。这些数据提供了大量证据,表明TSNIIA-SS是针对DXR诱发的心脏损伤的保护剂。

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