Journal of ethnopharmacology · 2025
Metabolism and Mendelian randomization study on the mechanism of Buyang Huanwu Decoction in regulating iron metabolism and improving cerebral ischemia-reperfusion injury.
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Xiong Tingting, Bai Yang, Shi Yiming, Li Yanling, Hu Zhongji, Duan Junxia, Lan Xiao, Ding Huang, Zhang Wei
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: BuYang HuanWu Decoction (BYHWD) is a classic prescription in traditional Chinese medicine that exerts anti-cerebral ischemia effects through multiple levels, targets, and pathways. However, its specific mechanism of action has not yet been fully clarified.
AIM OF THE STUDY: To investigate the mechanism by which BYHWD regulates iron metabolism and improves brain tissue damage following cerebral ischemia-reperfusion injury.
METHODS: A middle cerebral artery occlusion (MCAO) rat model was used to simulate ischemia-reperfusion, followed by BYHWD intervention. Neurological deficits were assessed using Longa and mNSS scores. Histopathological damage was evaluated by HE and Nissl staining. Inflammatory factors (IL-4, IL-10, TNF-α, IL-1β) were detected by ELISA, and immunofluorescence assessed IBA1, INOS and ARG1 expression. Oxidative stress was analyzed by measuring MDA 、T-AOC 、Fe2+levels. Western blot (WB) was used to detect iron metabolism-related proteins (TfR1, FPN1, DMT1, ACSL4, PTGS2). Non-targeted metabolomics identified the mechanism through which BYHWD regulates iron metabolism. GSH levels were measured, and WB assessed GPX4 expression. Mendelian randomization validated causal associations.
RESULTS: BYHWD alleviated neurological deficits, histopathological damage, inflammation, and oxidative stress. Metabolomics suggested a mechanism involving the "L-cysteine → GSH → GPX4" pathway, confirmed by Mendelian randomization analysis.
CONCLUSION: BYHWD improves iron metabolism, reducing inflammation and oxidative stress after ischemia-reperfusion, likely through cysteine upregulation, glutathione synthesis, GPX4 release, and lipid peroxidation inhibition.
AIM OF THE STUDY: To investigate the mechanism by which BYHWD regulates iron metabolism and improves brain tissue damage following cerebral ischemia-reperfusion injury.
METHODS: A middle cerebral artery occlusion (MCAO) rat model was used to simulate ischemia-reperfusion, followed by BYHWD intervention. Neurological deficits were assessed using Longa and mNSS scores. Histopathological damage was evaluated by HE and Nissl staining. Inflammatory factors (IL-4, IL-10, TNF-α, IL-1β) were detected by ELISA, and immunofluorescence assessed IBA1, INOS and ARG1 expression. Oxidative stress was analyzed by measuring MDA 、T-AOC 、Fe2+levels. Western blot (WB) was used to detect iron metabolism-related proteins (TfR1, FPN1, DMT1, ACSL4, PTGS2). Non-targeted metabolomics identified the mechanism through which BYHWD regulates iron metabolism. GSH levels were measured, and WB assessed GPX4 expression. Mendelian randomization validated causal associations.
RESULTS: BYHWD alleviated neurological deficits, histopathological damage, inflammation, and oxidative stress. Metabolomics suggested a mechanism involving the "L-cysteine → GSH → GPX4" pathway, confirmed by Mendelian randomization analysis.
CONCLUSION: BYHWD improves iron metabolism, reducing inflammation and oxidative stress after ischemia-reperfusion, likely through cysteine upregulation, glutathione synthesis, GPX4 release, and lipid peroxidation inhibition.