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Aloe-emodin relieves zidovudine-induced injury in neonatal rat ventricular myocytes by regulating the p90rsk/p-bad/bcl-2 signaling pathway
Environmental Toxicology and Pharmacology ( IF 4.3 ) Pub Date : 2020-11-05 , DOI: 10.1016/j.etap.2020.103540
Wei Zhao , Ye Yuan , Burong Feng , Yue Sun , Huiwei Jiang , Wei Zhao , Yuyang Zheng , Lihui Zhao , Tingting Chen , Yan Bai , Pengzhou Hang , Yingfu Chen , Zhimin Du

Background/Aims

Zidovudine (3′-azido-2′,3′-deoxythymidine; AZT) is a first-line drug for treatment of human immunodeficiency virus infection (HIV). However, its application is limited by cardiotoxicity due to cardiomyocyte injury. This study investigated whether Aloe-emodin (AE), an anthraquinone compound, protects against AZT-induced cardiomyocyte toxicity.

Methods

MTT, JC-1 assays and TUNEL were examined to verify the protective effect of AE against AZT-induced cardiomyocyte injury. Western blotting was performed to explore the anti-apoptotic effect of AE using anti-apoptotic proteins p90rsk, p-bad, and bcl-2 and pro-apoptotic proteins apaf-1, cleaved-caspase-3, and cytochrome c.

Results

We observed a protective effect of AE against cell viability decrease and TUNEL positive cells increase induced by AZT, which was counteracted by BI-D1870. Western blot analysis found that AE significantly inhibited cardiomyocyte apoptosis by activating p90rsk/p-bad/bcl-2 signaling pathway. Furthermore, BI-D1870 counteracted the anti-apoptotic effect of AE.

Conclusions

Taken together, these results indicate that AE attenuated AZT-induced cardiomyocyte apoptosis by activating p90rsk.



中文翻译:

芦荟大黄素通过调节p90rsk / p -bad / bcl-2信号通路减轻齐多夫定对新生大鼠心室肌细胞的损伤

背景/目标

齐多夫定(3'-azido-2',3'-脱氧胸苷; AZT)是用于治疗人类免疫缺陷病毒感染(HIV)的一线药物。然而,由于心肌细胞损伤,其应用受到心脏毒性的限制。这项研究调查了芦荟大黄素(AE),一种蒽醌化合物是否能抵抗AZT诱导的心肌细胞毒性。

方法

检查了MTT,JC-1分析和TUNEL,以验证AE对AZT诱导的心肌细胞损伤的保护作用。使用抗凋亡蛋白p90rsk,p -bad和bcl-2以及促凋亡蛋白apaf-1,cleaved-caspase-3和细胞色素c进行蛋白质印迹研究,探讨AE的抗凋亡作用。

结果

我们观察到AE对AZT诱导的细胞活力降低和TUNEL阳性细胞增加的保护作用,这被BI-D1870抵消。Western印迹分析发现,AE通过激活p90rsk / p -bad / bcl-2信号通路显着抑制心肌细胞凋亡。此外,BI-D1870抵消了AE的抗凋亡作用。

结论

综上所述,这些结果表明AE通过激活p90rsk减弱了AZT诱导的心肌细胞凋亡。

更新日期:2020-11-17
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