Gastrodin alleviates myocardial infarction by inhibiting inflammation, and apoptosis and promoting endothelial cell proliferation

IF 2.3 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Ruochen Du , Ying Guo , Wanting Zhong , Yuantao Gao , Miaomiao Xu , Chunfang Wang , Yitong Yuan
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引用次数: 0

Abstract

Gastrodin, a bioactive ingredient extracted from the Chinese herb Gastrodia gastrodia, has shown potential therapeutic effects in cardiovascular diseases, but its specific role in myocardial infarction is unclear. This study investigated the protective effect of gastrodin on myocardial infarction and its potential mechanism. By clamping the left coronary artery, we created a model of myocardial infarction in C57BL/6J mice. For 14 days, mice in the control and myocardial infarction groups received a daily dose of 100 mg/kg gastrodin. Gastrodin significantly improved cardiac dysfunction in mice with myocardial infarction, decreased heart weight/body weight (HW/BW) and heart weight/tibial length (HW/TL) ratios, and inhibited mRNA expression levels of cardiac fibrosis biomarkers (Collagen Type I (Col1), Collagen Type III (Col3), Matrix Metalloproteinase-2 (MMP-2), Matrix Metalloproteinase-9 (MMP-9)). In addition, gastrodin also inhibited the activity of apoptosis marker Caspase 3, decreased the Bax/Bcl2 mRNA ratio, decreased the expression of pro-inflammatory factors (Interleukin-1 beta (IL-1β), Tumor Necrosis Factor-alpha (TNF-α), Interleukin-6 (IL-6)) and pro-inflammatory adhesion molecule Monocyte Chemoattractant Protein-1 (MCP1), and promoted the expression of angiogenesis marker Cluster of Differentiation 31 (CD31). RNA sequencing and Rt-qPCR analysis showed that gastrodin treatment significantly up-regulated the expression of genes related to cell proliferation (Cyclin-Dependent Kinase 1 (CDK1), Threonine Tyrosine Kinase (TTK), Cyclin B2 (CCNB2), Polo-Like Kinase 1 (PLK1)), and promoted the proliferation of human aortic endothelial cells (HAECs). These findings suggest that gastrodin can effectively reduce the pathological changes of myocardial infarction by inhibiting inflammation, reducing apoptosis, and promoting endothelial cell proliferation, thus providing a new strategy for the prevention and treatment of myocardial infarction.
天麻素通过抑制炎症、细胞凋亡和促进内皮细胞增殖来减轻心肌梗死
天麻素是一种从中草药天麻中提取的生物活性成分,已显示出对心血管疾病的潜在治疗作用,但其在心肌梗死中的具体作用尚不清楚。本研究探讨天麻素对心肌梗死的保护作用及其可能机制。通过夹持左冠状动脉,建立C57BL/6J小鼠心肌梗死模型。对照组和心肌梗死组小鼠连续14天每天给药100 mg/kg天麻素。天麻素显著改善心肌梗死小鼠心功能障碍,降低心脏重量/体重(HW/BW)和心脏重量/胫骨长度(HW/TL)比,抑制心肌纤维化生物标志物(ⅰ型胶原(Col1)、ⅲ型胶原(Col3)、基质金属蛋白酶-2 (MMP-2)、基质金属蛋白酶-9 (MMP-9)) mRNA表达水平。此外,天麻素还能抑制凋亡标志物Caspase 3的活性,降低Bax/Bcl2 mRNA比值,降低促炎因子(白细胞介素-1β (IL-1β)、肿瘤坏死因子α (TNF-α)、白细胞介素-6 (IL-6))和促炎粘附分子单核细胞趋化蛋白-1 (MCP1)的表达,促进血管生成标志物分化簇31 (CD31)的表达。RNA测序和Rt-qPCR分析显示,天麻素处理可显著上调细胞增殖相关基因(细胞周期蛋白依赖性激酶1 (CDK1)、苏氨酸酪氨酸激酶(TTK)、细胞周期蛋白B2 (CCNB2)、pol - like激酶1 (PLK1))的表达,促进人主动脉内皮细胞(HAECs)的增殖。上述结果提示天麻素可通过抑制炎症、减少细胞凋亡、促进内皮细胞增殖等方式有效减轻心肌梗死的病理改变,为心肌梗死的防治提供了新的策略。
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来源期刊
Biochemistry and Biophysics Reports
Biochemistry and Biophysics Reports Biochemistry, Genetics and Molecular Biology-Biophysics
CiteScore
4.60
自引率
0.00%
发文量
191
审稿时长
59 days
期刊介绍: Open access, online only, peer-reviewed international journal in the Life Sciences, established in 2014 Biochemistry and Biophysics Reports (BB Reports) publishes original research in all aspects of Biochemistry, Biophysics and related areas like Molecular and Cell Biology. BB Reports welcomes solid though more preliminary, descriptive and small scale results if they have the potential to stimulate and/or contribute to future research, leading to new insights or hypothesis. Primary criteria for acceptance is that the work is original, scientifically and technically sound and provides valuable knowledge to life sciences research. We strongly believe all results deserve to be published and documented for the advancement of science. BB Reports specifically appreciates receiving reports on: Negative results, Replication studies, Reanalysis of previous datasets.
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