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Published on: March 29, 2017
Bupleurum chinense DC. reduces LPS-induced neuroinflammation in rats by activating CREB and suppressing NF-κB and
Huan-Huan Wang1, Bai-Jin Chang2, Yan-Ru Liu1
1Shaanxi Province Key Laboratory of New Drugs and Chinese Medicine Foundation Research, Shaanxi Collaborative Innovation Center Medicinal Resources Industrialization, Shaanxi University of Chinese Medicine, 712083, Xianyang, PR China.
Ethnopharmacological Relevance:
Bupleurum chinense DC., is traditionally used for "soothing the liver qi and relieving depression." In traditional Chinese medicine theory, liver qi stagnation is often associated with emotional disturbances and mental depression, which modern research suggests may involve the underlying neuroinflammatory processes. This study evaluated its anti-neuroinflammatory effects and identified key mechanisms to elucidate its traditional use.
Objective Of The Research:
This study aimed to examine the principal bioactive compounds in Bupleurum chinense DC. and their modulatory effects on neuroinflammation via the NF-κB, TNF-α, CREB signaling pathways.
Materials And Methods:
UPLC-MS/MS and network pharmacology were used to identify the chemical constituents and predict the anti-inflammatory targets of Bupleurum chinense DC. A lipopolysaccharide (LPS)-induced rat model was evaluated using an enzyme-linked immunosorbent assay (ELISA) and hematoxylin and eosin staining. Metabolomic analysis was performed to elucidate primary metabolic pathways. Subsequently, molecular docking, molecular dynamics simulations, Western blotting (WB), and reverse transcription quantitative polymerase chain reaction (RT-qPCR) were performed to validate the key components and targets.
Results:
Through UPLC-MS/MS analysis, saikosaponin A, quercetin, rutin, saikosaponin C, and saikosaponin D were identified as key active compounds in Bupleurum chinense DC. Experimental results from inflammatory rat models demonstrated that Bupleurum chinense DC. ameliorates LPS-induced neuroinflammation. Metabolomic analysis revealed biomarkers associated with the TNF-α signaling pathway and identified TNF-α, NF-κB, and CREB as core therapeutic targets. Molecular docking and dynamics simulations confirmed the stability of compound-target interactions. Finally, ELISA, WB and RT-qPCR analyses confirmed that Bupleurum chinense DC. modulates NF-κB, TNF-α, and CREB in a dose-dependent manner, thereby mechanistically establishing its neuroprotective effects.
Conclusion:
Bupleurum chinense DC. mitigated inflammation by upregulating CREB protein expression and downregulating NF-κB and TNF-α within the TNF-α signaling pathway.
