Chinese journal of integrative medicine · 2026
Mechanisms of Tianma Gouteng Yin in Treating Hypertension-Associated Vascular Cognitive Impairment: Insights from Experiments, Network Pharmacology, and Molecular Docking.
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Li Na-Chuan, Du Ya-Wei, Zhang Hong-Xiao, Zhao Fan-Ying, Yi Liu-Feng, Wang Xiang-Zhao, Liu Zi-Wang
Аннотация
OBJECTIVE: To evaluate active components of Tianma Gouteng Yin (TMGTY) and its mechanisms in treating hypertension-associated vascular cognitive impairment (VCI).
METHODS: Network pharmacology and molecular docking were used to identify major active ingredients and potential targets of TMGTY in treating hypertension-associated VCI. An in vivo model was established using spontaneously hypertensive rats subjected to unilateral common carotid artery occlusion and a high-salt diet. Rats were randomly divided into 7 groups by a simple randomization method: control, model, sham, low-, medium-, and high-dose TMGTY, and nimodipine groups (n=6). After 28 days of oral administration, blood pressure, behavioral studies, pathological staining, and molecular mechanisms were assessed via tail artery blood pressure monitoring, the morris water maze test, HE staining, immunofluorescence staining, ELISA, and Western blotting.
RESULTS: Network analysis identified quercetin, kaempferol, beta-sitosterol, and stigmasterol as key ingredients. Pathway enrichment analysis identified the NF-κB signaling pathway as a key pathway through which TMGTY antagonizes the development of hypertension combined with VCI. Core targets included glyceraldehyde-3-phosphate dehydrogenase (GAPDH), interleukin 6 (IL-6), insulin (INS), tumor necrosis factor (TNF), and tumor protein p53 (TP53), and molecular docking confirmed stable binding to TNF and INS. In vivo experiments demonstrated that TMGTY significantly enhanced cognitive performance and reduced blood pressure. Furthermore, it lowered the levels of pro-inflammatory factors (IL-1β, IL-6, TNF-α, Ang-II) and malondialdehyde (MDA), while elevating superoxide dismutase (SOD) expression (P<0.05 or P<0.01). Immunofluorescence staining further revealed that TMGTY treatment reduced the number of Iba1- and CD16-labeled microglia in the hippocampal CA1 region, thereby alleviating neuroinflammation. Additionally, TMGTY inhibited the expression levels of p-NF-κB p65/NF-κB p65 proteins and attenuated neuroinflammation.
CONCLUSION: TMGTY exerts multi-component, multi-target effects on hypertension-associated VCI, mitigating neuroinflammation and oxidative stress via modulation of NF-κB signaling pathway.
METHODS: Network pharmacology and molecular docking were used to identify major active ingredients and potential targets of TMGTY in treating hypertension-associated VCI. An in vivo model was established using spontaneously hypertensive rats subjected to unilateral common carotid artery occlusion and a high-salt diet. Rats were randomly divided into 7 groups by a simple randomization method: control, model, sham, low-, medium-, and high-dose TMGTY, and nimodipine groups (n=6). After 28 days of oral administration, blood pressure, behavioral studies, pathological staining, and molecular mechanisms were assessed via tail artery blood pressure monitoring, the morris water maze test, HE staining, immunofluorescence staining, ELISA, and Western blotting.
RESULTS: Network analysis identified quercetin, kaempferol, beta-sitosterol, and stigmasterol as key ingredients. Pathway enrichment analysis identified the NF-κB signaling pathway as a key pathway through which TMGTY antagonizes the development of hypertension combined with VCI. Core targets included glyceraldehyde-3-phosphate dehydrogenase (GAPDH), interleukin 6 (IL-6), insulin (INS), tumor necrosis factor (TNF), and tumor protein p53 (TP53), and molecular docking confirmed stable binding to TNF and INS. In vivo experiments demonstrated that TMGTY significantly enhanced cognitive performance and reduced blood pressure. Furthermore, it lowered the levels of pro-inflammatory factors (IL-1β, IL-6, TNF-α, Ang-II) and malondialdehyde (MDA), while elevating superoxide dismutase (SOD) expression (P<0.05 or P<0.01). Immunofluorescence staining further revealed that TMGTY treatment reduced the number of Iba1- and CD16-labeled microglia in the hippocampal CA1 region, thereby alleviating neuroinflammation. Additionally, TMGTY inhibited the expression levels of p-NF-κB p65/NF-κB p65 proteins and attenuated neuroinflammation.
CONCLUSION: TMGTY exerts multi-component, multi-target effects on hypertension-associated VCI, mitigating neuroinflammation and oxidative stress via modulation of NF-κB signaling pathway.