Zang Zhen-Zhong, Chen Li-Mei, Liu Yuan, Guan Yong-Mei, Du Qing, Xu Pan, Shen Qian, Yang Ming, Liu Hong-Ning, Liao Zheng-Gen
Key Laboratory of Modern Preparation of Chinese Medicine, Ministry of Education, Jiangxi University of Chinese Medicine, Nanchang, Jiangxi, China.
Jiangxi Province Key Laboratory of Chinese Medicine Etiopathogenisis, Jiangxi University of Chinese Medicine, Nanchang, Jiangxi, China.
Evid Based Complement Alternat Med. 2021 Jun 22;2021:6630795. doi: 10.1155/2021/6630795. eCollection 2021.
is a traditional aromatic resuscitation drug that can be clinically used to prevent cardiovascular diseases. The volatile oil of (VOA) possesses important medicinal properties, including protection against acute myocardial ischemia (MI) injury. However, the pharmacodynamic material basis and molecular mechanisms underlying this protective effect remain unclear. Using network pharmacology and animal experiments, we studied the mechanisms and pathways implicated in the activity of VOA against acute MI injury. First, VOA was extracted from three batches of using steam distillation, and then, its chemical composition was determined by GC-MS. Next, the components-targets and protein-protein interaction networks were constructed using systematic network pharmacology. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were also conducted in order to predict the possible pharmacodynamic mechanisms. Furthermore, animal experiments including ELISAs, histological examinations, and Western blots were performed in order to validate the pharmacological effects of VOA. In total, 33 chemical components were identified in VOA, and -asarone was found to be the most abundant component. Based on network pharmacology analysis, the therapeutic effects of VOA against myocardial ischemia might be mediated by signaling pathways involving COX-2, PPAR-, VEGF, and cAMP. Overall, the obtained results indicate that VOA alleviates the pathological manifestations of isoproterenol-hydrochloride-induced myocardial ischemia in rats, including the decreased SOD (superoxide dismutase) content and increased LDH (lactic dehydrogenase) content. Moreover, the anti-MI effect of VOA might be attributed to the downregulation of the COX-2 protein that inhibits apoptosis, the upregulation of the PPAR- protein that regulates energy metabolism, and the activation of VEGF and cAMP signaling pathways.
是一种传统的芳香开窍药物，临床上可用于预防心血管疾病。[药物名称]挥发油（VOA）具有重要的药用特性，包括对急性心肌缺血（MI）损伤的保护作用。然而，这种保护作用的药效物质基础和分子机制仍不清楚。我们利用网络药理学和动物实验，研究了VOA抗急性MI损伤活性所涉及的机制和途径。首先，采用水蒸气蒸馏法从三批[药物名称]中提取VOA，然后用气相色谱-质谱联用仪（GC-MS）测定其化学成分。接下来，运用系统网络药理学构建成分-靶点和蛋白质-蛋白质相互作用网络。还进行了基因本体论（GO）功能和京都基因与基因组百科全书（KEGG）通路富集分析，以预测可能的药效机制。此外，进行了包括酶联免疫吸附测定（ELISA）、组织学检查和蛋白质免疫印迹法（Western blot）在内的动物实验，以验证VOA的药理作用。总共在VOA中鉴定出33种化学成分，发现α-细辛脑是含量最高的成分。基于网络药理学分析，VOA对心肌缺血的治疗作用可能是通过涉及环氧化酶-2（COX-2）、过氧化物酶体增殖物激活受体-γ（PPAR-γ）、血管内皮生长因子（VEGF）和环磷酸腺苷（cAMP）的信号通路介导的。总体而言，所得结果表明VOA减轻了盐酸异丙肾上腺素诱导的大鼠心肌缺血的病理表现，包括超氧化物歧化酶（SOD）含量降低和乳酸脱氢酶（LDH）含量升高。此外，VOA的抗MI作用可能归因于抑制细胞凋亡的COX-2蛋白的下调、调节能量代谢的PPAR-γ蛋白的上调以及VEGF和cAMP信号通路的激活。
