Journal of ethnopharmacology · 2026
Mechanism of Buyang Huanwu Decoction in regulating arachidonic acid metabolism to mediate microglial polarization and alleviate cerebral ischemic injury.
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Zhao Yaqing, Xiong Tingting, Shi Yiming, Peng Lequn, Duan Junxia, Lu Jin, Zhang Qianxue, Fu Xinying, Ding Huang, Shang Hongcai, Zhang Wei
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: BYHWD, a classical prescription for post-stroke rehabilitation, protects against cerebral ischemia by modulating microglial polarization, oxidative stress, and lipid metabolism.
OBJECTIVE: To investigate the mechanism by which Buyang Huanwu Decoction regulates arachidonic acid metabolism to mediate microglial polarization and alleviate cerebral ischemic injury.
METHODS: The study employed a rat model of middle cerebral artery occlusion (MCAO) using SD rats, as well as oxygen-glucose deprivation/reoxygenation (OGD/R) models in bEnd.3 and BV.2 cells. The subjects received BYHWD treatment. The protective effects of BYHWD on brain tissue were evaluated using neurological function scoring, HE staining, immunofluorescence, ELISA, PCR, and biochemical assays. The effects of BYHWD on the function and morphology of microvascular endothelial cells were examined using immunofluorescence, tube formation assays, and cytoskeletal staining. Metabolomic profiling was performed to screen for differential metabolites and associated pathways involved in BYHWD-mediated improvement of lipid metabolism. The identified key targets were validated by a combination of Western blotting, immunofluorescence, and biochemical assays. Finally, Mendelian randomization analysis was employed to confirm the causal relationship.
RESULTS: In vivo and in vitro studies showed that BYHWD markedly improved neurological function and attenuated neuronal injury. The underlying mechanism involves the inhibition of arachidonic acid metabolism and the regulation of glycerophospholipid metabolism to restore lipid homeostasis, along with the attenuation of inflammatory responses and oxidative stress damage, as well as the promotion of cerebral microvascular repair. Mendelian randomization analysis further confirmed that lipid metabolic disturbances are a risk factor for large artery atherosclerosis stroke.
CONCLUSION: BYHWD protects against cerebral ischemia/reperfusion injury by blocking arachidonic acid metabolism, adjusting glycerophospholipid pathways to restore lipid homeostasis reducing inflammation and oxidative stress, and facilitating the restoration of injured blood vessels.
OBJECTIVE: To investigate the mechanism by which Buyang Huanwu Decoction regulates arachidonic acid metabolism to mediate microglial polarization and alleviate cerebral ischemic injury.
METHODS: The study employed a rat model of middle cerebral artery occlusion (MCAO) using SD rats, as well as oxygen-glucose deprivation/reoxygenation (OGD/R) models in bEnd.3 and BV.2 cells. The subjects received BYHWD treatment. The protective effects of BYHWD on brain tissue were evaluated using neurological function scoring, HE staining, immunofluorescence, ELISA, PCR, and biochemical assays. The effects of BYHWD on the function and morphology of microvascular endothelial cells were examined using immunofluorescence, tube formation assays, and cytoskeletal staining. Metabolomic profiling was performed to screen for differential metabolites and associated pathways involved in BYHWD-mediated improvement of lipid metabolism. The identified key targets were validated by a combination of Western blotting, immunofluorescence, and biochemical assays. Finally, Mendelian randomization analysis was employed to confirm the causal relationship.
RESULTS: In vivo and in vitro studies showed that BYHWD markedly improved neurological function and attenuated neuronal injury. The underlying mechanism involves the inhibition of arachidonic acid metabolism and the regulation of glycerophospholipid metabolism to restore lipid homeostasis, along with the attenuation of inflammatory responses and oxidative stress damage, as well as the promotion of cerebral microvascular repair. Mendelian randomization analysis further confirmed that lipid metabolic disturbances are a risk factor for large artery atherosclerosis stroke.
CONCLUSION: BYHWD protects against cerebral ischemia/reperfusion injury by blocking arachidonic acid metabolism, adjusting glycerophospholipid pathways to restore lipid homeostasis reducing inflammation and oxidative stress, and facilitating the restoration of injured blood vessels.