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鹿茸多肽-3.2KD通过TGF-β/SMAD信号通路改善阿霉素诱导的心肌损伤。

Pilose Antler Peptide-3.2KD Ameliorates Adriamycin-Induced Myocardial Injury Through TGF-β/SMAD Signaling Pathway.

作者信息

Xu Yan, Qu Xiaobo, Zhou Jia, Lv Guangfu, Han Dong, Liu Jinlong, Liu Yuexin, Chen Ying, Qu Peng, Huang Xiaowei

机构信息

School of Pharmaceutical, Changchun University of Chinese Medicine, Changchun, China.

Jilin Ginseng Academy, Changchun University of Chinese Medicine, Changchun, China.

出版信息

Front Cardiovasc Med. 2021 May 28;8:659643. doi: 10.3389/fcvm.2021.659643. eCollection 2021.

DOI:10.3389/fcvm.2021.659643
PMID:34124197
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8194399/
Abstract

Adriamycin (ADR)-based combination chemotherapy is the standard treatment for some patients with tumors in clinical, however, long-term application can cause dose-dependent cardiotoxicity. Pilose Antler, as a traditional Chinese medicine, first appeared in the Han Dynasty and has been used to treat heart disease for nearly a thousand years. Previous data revealed pilose antler polypeptide (PAP, 3.2KD) was one of its main active components with multiple biological activities for cardiomyopathy. PAP-3.2KD exerts protective effects againt myocardial fibrosis. The present study demonstrated the protective mechanism of PAP-3.2KD against Adriamycin (ADR)-induced myocardial injury through using animal model with ADR-induced myocardial injury. PAP-3.2KD markedly improved the weight increase and decreased the HW/BW index, heart rate, and ST height in ADR-induced groups. Additionally, PAP-3.2KD reversed histopathological changes (such as disordered muscle bundles, myocardial fibrosis and diffuse myocardial cellular edema) and scores of the heart tissue, ameliorated the myocardial fibrosis and collagen volume fraction through pathological examination, significantly increased the protein level of Bcl-2, and decreased the expression levels of Bax and caspase-3 in myocardial tissue by ELISA, compared to those in ADR-induced group. Furthermore, ADR stimulation induced the increased protein levels of TGF-β1 and SMAD2/3/4, the increased phosphorylation levels of SMAD2/3 and the reduced protein levels of SMAD7. The expression levels of protein above in ADR-induced group were remarkably reversed in PAP-3.2KD-treated groups. PAP-3.2KD ameliorated ADR-induced myocardial injury by regulating the TGF-β/SMAD signaling pathway. Thus, these results provide a strong rationale for the protective effects of PAP against ADR-induced myocardial injury, when ADR is used to treat cancer.

摘要

基于阿霉素（ADR）的联合化疗是临床上一些肿瘤患者的标准治疗方法，然而，长期应用会导致剂量依赖性心脏毒性。鹿茸作为一种传统中药，最早出现在汉代，用于治疗心脏病已有近千年历史。先前的数据显示，鹿茸多肽（PAP，3.2KD）是其主要活性成分之一，对心肌病具有多种生物学活性。PAP-3.2KD对心肌纤维化具有保护作用。本研究通过使用ADR诱导心肌损伤的动物模型，证明了PAP-3.2KD对ADR诱导的心肌损伤的保护机制。PAP-3.2KD显著改善了ADR诱导组的体重增加，并降低了HW/BW指数、心率和ST段高度。此外，通过病理检查，PAP-3.2KD逆转了心脏组织的组织病理学变化（如肌束紊乱、心肌纤维化和弥漫性心肌细胞水肿）和评分，改善了心肌纤维化和胶原体积分数，通过ELISA法显著提高了心肌组织中Bcl-2的蛋白水平，并降低了Bax和caspase-3的表达水平，与ADR诱导组相比。此外，ADR刺激导致TGF-β1和SMAD2/3/4的蛋白水平升高，SMAD2/3的磷酸化水平升高，SMAD7的蛋白水平降低。在PAP-3.2KD治疗组中，ADR诱导组上述蛋白的表达水平显著逆转。PAP-3.2KD通过调节TGF-β/SMAD信号通路改善ADR诱导的心肌损伤。因此，这些结果为鹿茸在ADR用于治疗癌症时对ADR诱导的心肌损伤的保护作用提供了有力的理论依据。

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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d7e/8194399/85e02234952a/fcvm-08-659643-g0008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d7e/8194399/a3ed2f9157b1/fcvm-08-659643-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d7e/8194399/0691af60985f/fcvm-08-659643-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d7e/8194399/d830535df0ab/fcvm-08-659643-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d7e/8194399/6d8fa04c925f/fcvm-08-659643-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d7e/8194399/4fe2cc1f6d7e/fcvm-08-659643-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d7e/8194399/8b812dc957d6/fcvm-08-659643-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d7e/8194399/85e02234952a/fcvm-08-659643-g0008.jpg

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