Spinal cord injury (SCI) is defined as damage to the spinal cord that temporarily or permanently changes its function. There is no definite treatment established for neurological complete injury patients. This study investigated the effect of ginseng extract and ginsenosides on neurological recovery and antioxidant efficacies in rat models following SCI and explore the appropriate dosage. Searches were done on PubMed, Embase, and Chinese databases, and animal studies matches the inclusion criteria were selected. Pair-wise meta-analysis and subgroup analysis were performed. Ten studies were included, and the overall methodological qualities were low quality. The result showed ginseng extract and ginsenosides significantly improve neurological function, through the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale (pooled MD = 4.40; 95% CI = 3.92 to 4.88; p < 0.00001), significantly decrease malondialdehyde (MDA) (n = 290; pooled MD = −2.19; 95% CI = −3.16 to −1.22; p < 0.0001) and increase superoxide dismutase (SOD) levels (n = 290; pooled MD = 2.14; 95% CI = 1.45 to 2.83; p < 0.00001). Both low (<25 mg/kg) and high dosage (≥25 mg/kg) showed significant improvement in the motor function recovery in SCI rats. Collectively, this review suggests ginseng extract and ginsenosides has a protective effect on SCI, with good safety and a clear mechanism of action and may be suitable for future clinical trials and applications.
Background. Qi She Pill (QSP) is a traditional prescription for the treatment of neuropathic pain (NP) that is widely used in China. However, no network pharmacology studies of QSP in the treatment of NP have been conducted to date. Objective. To verify the potential pharmacological effects of QSP on NP, its components were analyzed via target docking and network analysis, and network pharmacology methods were used to study the interactions of its components. Materials and Methods. Information on pharmaceutically active compounds in QSP and gene information related to NP were obtained from public databases, and a compound-target network and protein-protein interaction network were constructed to study the mechanism of action of QSP in the treatment of NP. The mechanism of action of QSP in the treatment of NP was analyzed via Gene Ontology (GO) biological process annotation and Kyoto Gene and Genomics Encyclopedia (KEGG) pathway enrichment, and the drug-like component-target-pathway network was constructed. Results. The compound-target network contained 60 compounds and 444 corresponding targets. The key active compounds included quercetin and beta-sitosterol. Key targets included PTGS2 and PTGS1. The protein-protein interaction network of the active ingredients of QSP in the treatment of NP featured 48 proteins, including DRD2, CHRM, β2-adrenergic receptor, HTR2A, and calcitonin gene-related peptide. In total, 53 GO entries, including 35 biological process items, 7 molecular function items, and 11 cell related items, were identified. In addition, eight relevant (KEGG) pathways were identified, including calcium, neuroactive ligand-receptor interaction, and cAMP signaling pathways. Conclusion. Network pharmacology can help clarify the role and mechanism of QSP in the treatment of NP and provide a foundation for further research.
Background: Shenqisherong pill (SQSRP) has been used clinically to treat cervical spondylotic myelopathy (CSM) with satisfactory results; however, its active ingredients and mechanisms are unclear. The present study aimed to explore the active ingredients and molecular mechanisms of SQSRP against CSM using network pharmacology and molecular docking.
Methods:The compounds in SQSRP were obtained from public databases and related literature, and oral bioavailability (≥30%) and drug-likeness (≥0.18) were screened using absorption, distribution, metabolism, and excretion (ADME) criteria. Compounds-related and CSM-related target genes were identified using public databases, and the overlapping genes between compounds and CSM target genes were identified using a Venn diagram. Cytoscape and STRING were used to construct, visualize, and analyze the interaction network between these overlapping targets. Gene Ontology (GO) and KEGG pathway enrichment analysis of overlapping targets used Omicshare tools and constructed a compound-overlapping targets network, target-pathway network, and compound-target-pathway network using Cytoscape. Finally, molecular docking software was used to verify the targets.Results: A total of 447 compounds in SQSRP were identified, and ADME screening identified 96 compounds as potentially active ingredients. A total of 249 compound-related genes and 280 CSMrelated genes were identified using public databases, and 53 overlapping genes were identified. The results of compound targets and protein-protein interaction network analysis showed that the pharmacological effects of SQSRP against CSM involved 56 compounds and 53 genes. The results of GO and KEGG pathway enrichment analysis suggested that the therapeutic effects of SQSRP against CSM were exerted by reducing inflammation, inhibiting apoptosis, and protecting neurons. The molecular mechanisms may be strongly associated with PI3K-Akt, MAPK, IL-17, and TNF, which might be pivotal signaling pathways.
Conclusions:The active ingredients and mechanisms of SQSRP against CSM were investigated using network pharmacology. The findings proved that the pill could treat CSM through multi-component, multitarget, and multi-pathway synergy and provide a theoretical basis for the subsequent extraction of active ingredients from SQSRP.
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