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Abstract Title:

Aloe-emodin relieves zidovudine-induced injury in neonatal rat ventricular myocytes by regulating the p90rsk/p-bad/bcl-2 signaling pathway.

Abstract Source:

Environ Toxicol Pharmacol. 2021 Jan ;81:103540. Epub 2020 Nov 5. PMID: 33161113

Abstract Author(s):

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

Article Affiliation:

Wei Zhao

Abstract:

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.

Study Type : Animal Study

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