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两种从 Linn. 中提取的生物碱对阿霉素诱导的 H9c2 心肌细胞毒性的保护作用。

Protective Effect of Two Alkaloids from Linn. against Doxorubicin-Induced Toxicity in H9c2 Cardiomyoblasts.

机构信息

Department of Life Sciences and Health, QiuZhen College, Huzhou University, Huzhou 313000, China.

CAS Key Laboratory of Tibetan Medicine Research, Northwest Institute of Plateau Biology, Xining 810008, China.

出版信息

Molecules. 2021 Mar 30;26(7):1946. doi: 10.3390/molecules26071946.

DOI:10.3390/molecules26071946
PMID:33808398
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8037594/
Abstract

BACKGROUND

Doxorubicin (Dox) is one of the most frequently prescribed anti-cancer drugs. However, clinical application with Dox is limited due to its potentially fatal cumulative cardiotoxicity. N--coumaroyl-4-aminobutan-1-ol (alk-A), an organic amide alkaloid and hippophamide (alk-B), a rare pyridoindole alkaloid were successfully obtained by purification and separation of seabuckthorn seed residue in our previous research. This study was undertaken to investigate the protective effect of alk-A and alk-B against Dox-induced embryonic rat cardiac cells (H9c2 cells) apoptosis.

METHODS

H9c2 cells were treated with Dox (2.5 µM) in the presence of alk-A and alk-B (10, 20, and 40 µM) and incubated for 24 h.

RESULTS

It was shown that pretreatment of the H9c2 cells with alk-A and alk-B significantly reduced Dox-induced apoptosis. Alk-A and alk-B both inhibited reactive oxygen species (ROS) production and suppressed cleaved-caspase-3 protein expression and the activation of JNK (Jun N-terminal kinases), as well as increasing ATP levels, favoring mitochondrial mitofusin protein expression, and relieving damage to mitochondrial DNA.

CONCLUSIONS

These results suggest that alk-A and alk-B can inhibit Dox-induced apoptosis in H9C2 cardiac muscle cells via inhibition of cell apoptosis and improvement of mitochondrial function, while alk-B showed more protection. Alk-B could be a potential candidate agent for protecting against cardiotoxicity in Dox-exposed patients.

摘要

背景

阿霉素（Dox）是最常被开的抗癌药物之一。然而，由于其潜在的致命累积性心脏毒性，临床应用受到限制。在我们之前的研究中，通过对沙棘种子残渣的纯化和分离，成功获得了 N-- 咖啡酰基-4-氨基丁醇（alk-A）和 hippophamide（alk-B），这是一种有机酰胺生物碱和一种罕见的吡啶并吲哚生物碱。本研究旨在探讨 alk-A 和 alk-B 对阿霉素诱导的胚胎大鼠心肌细胞（H9c2 细胞）凋亡的保护作用。

方法

用 Dox（2.5 µM）处理 H9c2 细胞，并在存在 alk-A 和 alk-B（10、20 和 40 µM）的情况下孵育 24 小时。

结果

结果表明，H9c2 细胞用 alk-A 和 alk-B 预处理可显著减少 Dox 诱导的细胞凋亡。alk-A 和 alk-B 均抑制活性氧（ROS）的产生，并抑制裂解的 caspase-3 蛋白表达和 JNK（Jun N-末端激酶）的激活，同时增加 ATP 水平，促进线粒体融合蛋白的表达，并减轻线粒体 DNA 的损伤。

结论

这些结果表明，alk-A 和 alk-B 可以通过抑制细胞凋亡和改善线粒体功能来抑制 Dox 诱导的 H9C2 心肌细胞凋亡，而 alk-B 显示出更强的保护作用。alk-B 可能是预防 Dox 暴露患者心脏毒性的潜在候选药物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/d03149342fd6/molecules-26-01946-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/e513bf626d67/molecules-26-01946-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/edc1375051e2/molecules-26-01946-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/81980fd2eed4/molecules-26-01946-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/f8ee10d88227/molecules-26-01946-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/fbde65a3c0b2/molecules-26-01946-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/9be229993822/molecules-26-01946-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/7e47902e4303/molecules-26-01946-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/d03149342fd6/molecules-26-01946-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/e513bf626d67/molecules-26-01946-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/edc1375051e2/molecules-26-01946-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/81980fd2eed4/molecules-26-01946-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/f8ee10d88227/molecules-26-01946-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/fbde65a3c0b2/molecules-26-01946-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/9be229993822/molecules-26-01946-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/7e47902e4303/molecules-26-01946-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e6e8/8037594/d03149342fd6/molecules-26-01946-g008.jpg

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