Effect of Tetrastigma hemsleyanum on sepsis and mechanism based on network pharmacology and experimental verification.
10.19540/j.cnki.cjcmm.20220523.401
- Author:
Jing-Ru ZHENG
1
;
Chun-Lian JI
2
;
Liang-Hui ZHAN
3
;
Jin-Bao PU
3
;
Li YAO
1
Author Information
1. College of Pharmaceutical Sciences, Zhejiang Chinese Medical University Hangzhou 310053, China.
2. Tongde Hospital of Zhejiang Province Hangzhou 310014, China.
3. Tongde Hospital of Zhejiang Province Hangzhou 310014, China Zhejiang Academy of Traditional Chinese Medicine Hangzhou 310014, China.
- Publication Type:Journal Article
- Keywords:
Tetrastigma hemsleyanum;
inflammation;
network pharmacology;
sepsis
- MeSH:
Animals;
Anti-Inflammatory Agents/therapeutic use*;
C-Reactive Protein;
Caspase 3/metabolism*;
Interleukin-10;
Interleukin-6/metabolism*;
Lactate Dehydrogenases/metabolism*;
Myeloblastin/metabolism*;
Myeloid Differentiation Factor 88/metabolism*;
NF-kappa B/metabolism*;
Network Pharmacology;
Procalcitonin/therapeutic use*;
Sepsis/genetics*;
Toll-Like Receptor 4/metabolism*;
Tumor Necrosis Factor-alpha/metabolism*;
bcl-2-Associated X Protein/metabolism*
- From:
China Journal of Chinese Materia Medica
2022;47(17):4744-4754
- CountryChina
- Language:Chinese
-
Abstract:
Based on network pharmacology and in vivo experiment, this study explored the therapeutic effect of Tetrastigma hemsle-yanum(SYQ) on sepsis and the underlying mechanism. The common targets of SYQ and sepsis were screened out by network pharmacology, and the "SYQ-component-target-sepsis" network was constructed. The protein-protein interaction(PPI) network was established by STRING. Gene Ontology(GO) term enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment were performed based on DAVID to predict the anti-sepsis mechanism of SYQ. The prediction results of network pharmacology were verified by animal experiment. The network pharmacology results showed that the key anti-sepsis targets of SYQ were tumor necrosis factor(TNF), interleukin(IL)-6, IL-1β, IL-10, and cysteinyl asparate specific proteinase 3(caspase-3), which were mainly involved in Toll-like receptor 4(TLR4)/myeloid differentiation factor 88(MyD88)/nuclear factor kappaB(NF-κB) signaling pathway. The results of animal experiment showed that SYQ can decrease the content of C-reactive protein(CRP), procalcitonin(PCT), lactate dehydrogenase(LDH), IL-6, TNF-α, and IL-1β, increase the content of IL-10, and down-regulate the protein levels of Bcl-2-associa-ted X(Bax)/B-cell lymphoma 2(Bcl2), cleaved caspase-3, TLR4, MyD88, and p-NF-κB p65/NF-κB p65. In summary, SYQ plays an anti-inflammatory role in the treatment of sepsis by acting on the key genes related to inflammation and apoptosis, such as TNF-α, IL-6, IL-lβ, IL-10, Bax, Bcl2, and cleaved caspase-3. The mechanism is the likelihood that it suppresses the TLR4/MyD88/NF-κB signaling pathway, which verifies relative prediction results of network pharmacology.
