School of Traditional Chinese Medicine, Beijing Key Lab of TCM Collateral Disease Theory Research, Capital Medical University, Beijing 100069, China.
Core Facility Center, Capital Medical University, Beijing 100069, China.
Mediators Inflamm. 2022 Jul 12;2022:9241261. doi: 10.1155/2022/9241261. eCollection 2022.
The potential active ingredients and corresponding potential targets of BSYS Capsule were obtained from the TCMSP, BATMAN-TCM, Swiss Target Prediction platform, and literature research. Disease targets of CNSD were explored through the GeneCards and the DisGeNET databases. The matching targets of BSYS in CNSD were identified from a Venn diagram. The protein-protein interaction (PPI) network was constructed using bioinformatics methods. Gene Ontology (GO) function and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed to predict the mechanisms of BSYS. Furthermore, the neuroprotective effects of BSYS were evaluated using a cell model of hydrogen peroxide- (HO-) induced cell death in OLN-93 cells.
A total of 59 potential bioactive components of BSYS Capsule and 227 intersection targets were obtained. Topological analysis showed that AKT had the highest connectivity degrees in the PPI network. Enrichment analysis revealed that the targets of BSYS in the treatment of CNSD were the PI3K-Akt and MAPK signaling pathway, among other pathways. GO analysis results showed that the targets were associated with various biological processes, including apoptosis, reactive oxygen species metabolic process, and response to oxidative stress, among others. The experimental results demonstrated that BSYS drug-containing serum alleviated the HO-induced increase in LDH, MDA, and ROS levels and reversed the decrease in SOD and mitochondrial membrane potential induced by HO. BSYS treatment also decreased the number of TUNEL (+) cells, downregulated Bcl-2 expression, and upregulated Bax and c-caspase-3 expression by promoting Akt phosphorylation.
BSYS Capsule alleviated HO-induced OLN-93 cell injury by increasing Akt phosphorylation to suppress oxidative stress and cell apoptosis. Therefore, BSYS can be potentially used for CNSD treatment. However, the results of this study are only derived from in vitro experiments, lacking the validation of in vivo animal models, which is a limitation of our study. We will further verify the underlying mechanisms of BSYS in animal experiments in the future.
从 TCMSP、BATMAN-TCM、SwissTargetPrediction 平台和文献研究中获取 BSYS 胶囊的潜在活性成分和相应的潜在靶点。通过 GeneCards 和 DisGeNET 数据库探索 CNSD 的疾病靶点。从 Venn 图中确定 BSYS 与 CNSD 的匹配靶点。使用生物信息学方法构建蛋白质-蛋白质相互作用（PPI）网络。进行基因本体（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 BSYS 的作用机制。此外，使用过氧化氢（HO-）诱导的 OLN-93 细胞死亡细胞模型评估 BSYS 的神经保护作用。
共获得 59 种 BSYS 胶囊的潜在生物活性成分和 227 个交集靶点。拓扑分析显示，PPI 网络中 AKT 的连接度最高。富集分析显示，BSYS 治疗 CNSD 的靶点是 PI3K-Akt 和 MAPK 信号通路等其他通路。GO 分析结果表明，这些靶点与各种生物学过程有关，包括细胞凋亡、活性氧物质代谢过程和对氧化应激的反应等。实验结果表明，BSYS 含药血清减轻了 HO 诱导的 LDH、MDA 和 ROS 水平升高，并逆转了 HO 诱导的 SOD 和线粒体膜电位降低。BSYS 处理还通过促进 Akt 磷酸化降低 TUNEL（+）细胞数量，下调 Bcl-2 表达，上调 Bax 和 c-caspase-3 表达，从而抑制细胞凋亡。
BSYS 胶囊通过增加 Akt 磷酸化抑制氧化应激和细胞凋亡，缓解 HO 诱导的 OLN-93 细胞损伤。因此，BSYS 可用于 CNSD 的治疗。然而，本研究的结果仅来自体外实验，缺乏体内动物模型的验证，这是我们研究的一个局限性。我们将在未来的动物实验中进一步验证 BSYS 的潜在作用机制。
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