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砷剂诱导的心脏毒性通过丹酚酸 A 维持钙稳态和抑制内质网应激来减轻。

The Cardiotoxicity Induced by Arsenic Trioxide is Alleviated by Salvianolic Acid A via Maintaining Calcium Homeostasis and Inhibiting Endoplasmic Reticulum Stress.

机构信息

Beijing Key Laboratory of Innovative Drug Discovery of Traditional Chinese Medicine (Natural Medicine) and Translational Medicine, Institute of Medicinal Plant Development, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing 100193, China.

Key Laboratory of Bioactive Substances and Resource Utilization of Chinese Herbal Medicine, Ministry of Education, Beijing 100193, China.

出版信息

Molecules. 2019 Feb 2;24(3):543. doi: 10.3390/molecules24030543.

DOI:10.3390/molecules24030543
PMID:30717322
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6384753/
Abstract

Arsenic trioxide (ATO) has been verified as a breakthrough with respect to the management of acute promyelocytic leukemia (APL) in recent decades but associated with some serious adverse phenomena, particularly cardiac functional abnormalities. Salvianolic acid A (Sal A) is a major effective component in treating ATO-induced cardiotoxicity. Therefore, the objective of our study was to assess whether Sal A had protective effects by the regulation of calcium homeostasis and endoplasmic reticulum (ER) stress. For the in vivo study, BALB/c mice were treated with ATO and/or Sal A via daily tail vein injections for two weeks. For the in vitro study, we detected the effects of ATO and/or Sal A in real time using adult rat ventricular myocytes (ARVMs) and an IonOptix MyoCam system. Our results showed that Sal A pretreatment alleviated cardiac dysfunction and Ca overload induced by ATO in vivo and vitro. Moreover, Sal A increased sarcoplasmic reticulum (SR) Ca-ATPase (SERCA) activity and expression, alleviated [Ca]ER depletion, and decreased ER stress-related protein expression. Sal A protects the heart from ATO-induced injury and its administration correlates with the modulation of SERCA, the recovery of Ca homeostasis, and the down-regulation of ER stress-mediated apoptosis.

摘要

三氧化二砷（ATO）在近几十年来被证实是治疗急性早幼粒细胞白血病（APL）的突破，但它与一些严重的不良反应有关，特别是心脏功能异常。丹酚酸 A（Sal A）是治疗 ATO 诱导的心脏毒性的主要有效成分。因此，我们的研究目的是评估 Sal A 是否通过调节钙稳态和内质网（ER）应激来发挥保护作用。在体内研究中，BALB/c 小鼠通过每日尾静脉注射 ATO 和/或 Sal A 进行为期两周的治疗。在体外研究中，我们使用成年大鼠心室肌细胞（ARVMs）和 IonOptix MyoCam 系统实时检测 ATO 和/或 Sal A 的作用。我们的结果表明，Sal A 预处理可减轻体内和体外 ATO 诱导的心脏功能障碍和 Ca 超载。此外，Sal A 增加肌浆网（SR）Ca-ATPase（SERCA）活性和表达，减轻[Ca]ER 耗竭，并降低 ER 应激相关蛋白的表达。Sal A 可保护心脏免受 ATO 诱导的损伤，其给药与 SERCA 的调节、钙稳态的恢复和 ER 应激介导的凋亡下调相关。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/5601e863e79a/molecules-24-00543-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/8b0808f52296/molecules-24-00543-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/d99369cf088f/molecules-24-00543-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/b4010ffbbf29/molecules-24-00543-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/313c250bcd0f/molecules-24-00543-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/d7e85f1bedde/molecules-24-00543-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/2e6564f0abe6/molecules-24-00543-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/5601e863e79a/molecules-24-00543-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/8b0808f52296/molecules-24-00543-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/d99369cf088f/molecules-24-00543-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/b4010ffbbf29/molecules-24-00543-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/313c250bcd0f/molecules-24-00543-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/d7e85f1bedde/molecules-24-00543-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/2e6564f0abe6/molecules-24-00543-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d3bf/6384753/5601e863e79a/molecules-24-00543-g007.jpg

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