Tanshinone IIA attenuates cerebral-ischemia-reperfusion-induced neuroinflammation.
Tanshinone IIA attenuates cerebral-ischemia-reperfusion-induced neuroinflammation by inhibiting the TLR4/NF-κB signaling cascade: A study integrating network pharmacology, bioinformatics, and experimental validation.
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Abstract
BACKGROUND: Tanshinone IIA is the primary compound of Salvia miltiorrhiza, has neuroprotective and antioxidant properties. However, its anti-inflammatory role in cerebral ischemia-reperfusion injury is not well understood. PURPOSE: To determine whether Tanshinone IIA alleviates inflammation in CIRI via the TLR4/NF-κB signaling pathway. METHODS: Bioinformatics and network pharmacology analysis revealedCIRI-related targets of Tanshinone IIA. Furthermore, CytoHubba was employed to assess the Protein-protein interaction networks and hub targets. Moreover, molecular docking and 100 ns molecular dynamics simulations assessed Tanshinone IIA binding to core proteins. For in vivo, an MCAO/R rat model, and in vitro, OGD/R-injured HUVECs were used to evaluate neurological function, infarct size, histopathology (TTC, HE, TUNEL), cytokine levels (ELISA), and molecular markers (RT-qPCR, Western blot). RESULTS: The data revealed 10 hub targets including TLR4 and NFKB1, which were enriched in inflammatory pathways such as the "Toll-like receptor signaling pathway" and "NF-κB signaling pathway". Furthermore, it was observed that Tanshinone IIA stably interacted with TLR4/NFKB1 (binding energy
Affiliation
Chenxi Zhou
External References
- PubMed ID:
- 41265260
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