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基于网络药理学探讨参麦注射液对PC12细胞氧化应激损伤的神经保护作用

The Neuroprotective Effect of Shenmai Injection on Oxidative Stress Injury in PC12 Cells Based on Network Pharmacology.

作者信息

Wu Jing, Wu Jiang, Li Zhonghao, Dong Xiaoke, Yuan Siyuan, Liu Jinmin, Wang Le

机构信息

Beijing University of Chinese Medicine, Beijing 100029, China.

Dongfang Hospital Beijing University of Chinese Medicine, Beijing 100078, China.

出版信息

Evid Based Complement Alternat Med. 2022 May 27;2022:6969740. doi: 10.1155/2022/6969740. eCollection 2022.

DOI:10.1155/2022/6969740
PMID:35668778
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9166949/
Abstract

BACKGROUND

Shenmai injection (SMI) has been used in the treatment of cerebrovascular diseases and cardiovascular diseases. However, the underlying mechanism of SMI for neuroprotection after acute ischemic stroke (AIS) remains unclear. This study aimed to explore the potential molecular mechanism of SMI in treating reperfusion injury after AIS and its protective effect on PC12 cells against oxidative stress through in vitro experiments based on network pharmacological predictions.

METHODS

The network pharmacology method was used to collect the compounds in SMI and AIS damage targets, construct the "drug-disease" target interaction network diagram, screen the core targets, and predict the potential mechanism of SMI treatment of AIS. In addition, the oxidative stress model of PC12 cells was induced by HO to evaluate the neuroprotective effect and predictive mechanism of SMI on PC12 cells.

RESULTS

A component-targeted disease and functional pathway network showed that 24 components from SMI regulated 77 common targets shared by SMI and AIS. In PC12 cells damaged by HO, SMI increased cell survival, alleviated oxidative stress injury, prevented cell apoptosis, and increased the expression of APJ, AMPK, and p-GSK-3. After Si-APJ silenced APJ expression, the above protective effect of SMI was significantly weakened.

CONCLUSION

SMI is characterized by multiple components, multiple targets, and multiple pathways and inhibits oxidative stress and alleviates nerve injury induced by HO through regulating the APJ/AMPK/GSK-3 pathway.

摘要

背景

参麦注射液（SMI）已用于治疗脑血管疾病和心血管疾病。然而，参麦注射液对急性缺血性脑卒中（AIS）后神经保护的潜在机制仍不清楚。本研究旨在基于网络药理学预测，通过体外实验探讨参麦注射液治疗AIS后再灌注损伤的潜在分子机制及其对PC12细胞抗氧化应激的保护作用。

方法

采用网络药理学方法收集参麦注射液中的化合物及AIS损伤靶点，构建“药物-疾病”靶点相互作用网络图，筛选核心靶点，预测参麦注射液治疗AIS的潜在机制。此外，用HO诱导PC12细胞氧化应激模型，评价参麦注射液对PC12细胞的神经保护作用及预测机制。

结果

成分-靶点-疾病与功能通路网络显示，参麦注射液的24种成分调控了参麦注射液与AIS共有的77个共同靶点。在HO损伤的PC12细胞中，参麦注射液提高细胞存活率，减轻氧化应激损伤，防止细胞凋亡，并增加APJ、AMPK和p-GSK-3的表达。Si-APJ沉默APJ表达后，参麦注射液的上述保护作用明显减弱。

结论

参麦注射液具有多成分、多靶点、多途径的特点，通过调节APJ/AMPK/GSK-3通路抑制氧化应激，减轻HO诱导的神经损伤。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/d56395d3f411/ECAM2022-6969740.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/5236d5947f8d/ECAM2022-6969740.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/77618c670aa4/ECAM2022-6969740.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/dc6ccac57479/ECAM2022-6969740.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/731511281c24/ECAM2022-6969740.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/758ba95abba7/ECAM2022-6969740.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/1218a039a633/ECAM2022-6969740.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/d56395d3f411/ECAM2022-6969740.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/5236d5947f8d/ECAM2022-6969740.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/77618c670aa4/ECAM2022-6969740.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/dc6ccac57479/ECAM2022-6969740.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/731511281c24/ECAM2022-6969740.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/758ba95abba7/ECAM2022-6969740.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/1218a039a633/ECAM2022-6969740.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/af1b/9166949/d56395d3f411/ECAM2022-6969740.007.jpg

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