Journal of ethnopharmacology · 2026
Tongmai Yizhi Decoction Improves Post-Stroke Cognitive Impairment by Inhibiting Monoamine Oxidase to Reduce Dopamine Metabolism.
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Gao Ya-Qing, Wang Yi-Ran, Wang Yu, Liu Zhen-Ling, Zhang Kai-Xin, Ding Peng-Li, Hu Feng-Xian, Liu Wei, Tao Yi, Jia Qing-Yue, Wu Hong-Yun, Cui Wen-Qiang, Xu Xiang-Qing
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Tongmai Yizhi Decoction (TMYZD), a classic Chinese ethnomedical formula derived from Danggui Shaoyao San and Shenghui Decoction, has long been used for post-stroke amnesia and dementia as it activates blood circulation, tonifies kidney essence, resolves phlegm, and opens cerebral orifices. Its clinical efficacy against post-stroke cognitive impairment (PSCI) is verified, but the underlying pharmacological mechanisms remain unclear.
AIM OF THE STUDY: This study aimed to investigate the protective effect of TMYZD against PSCI and verify whether it acts via modulating the dopamine metabolic pathway to elucidate its molecular targets and pharmacological basis.
MATERIALS AND METHODS: Network pharmacology was applied to predict therapeutic targets, and metabolomics combined with mass spectrometry was used to identify regulated pathways. In vivo, middle cerebral artery occlusion/reperfusion rats were assessed for cognitive function, synaptic ultrastructure, and key target proteins. In vitro, HT22 cells under oxygen-glucose deprivation/reoxygenation with monoamine oxidase-B (MAOB) overexpression were used for target validation.
RESULTS: PSCI rats exhibited severe cognitive decline and synaptic structural damage. Monoamine oxidase-A (MAOA) and MAOB were identified as core therapeutic targets. TMYZD significantly regulated the dopamine pathway, upregulated tyrosine hydroxylase and dopamine receptor D2, downregulated MAOA/MAOB, and ameliorated synaptic injury. MAOB overexpression partially abolished the neuroprotective effect of TMYZD, confirming MAOB as a key target.
CONCLUSIONS: TMYZD improves cognitive function in PSCI by regulating dopamine metabolism, elevating dopamine levels, and enhancing synaptic plasticity, with MAOB as a critical target. These findings provide scientific evidence for the ethnomedical application of TMYZD in PSCI.
AIM OF THE STUDY: This study aimed to investigate the protective effect of TMYZD against PSCI and verify whether it acts via modulating the dopamine metabolic pathway to elucidate its molecular targets and pharmacological basis.
MATERIALS AND METHODS: Network pharmacology was applied to predict therapeutic targets, and metabolomics combined with mass spectrometry was used to identify regulated pathways. In vivo, middle cerebral artery occlusion/reperfusion rats were assessed for cognitive function, synaptic ultrastructure, and key target proteins. In vitro, HT22 cells under oxygen-glucose deprivation/reoxygenation with monoamine oxidase-B (MAOB) overexpression were used for target validation.
RESULTS: PSCI rats exhibited severe cognitive decline and synaptic structural damage. Monoamine oxidase-A (MAOA) and MAOB were identified as core therapeutic targets. TMYZD significantly regulated the dopamine pathway, upregulated tyrosine hydroxylase and dopamine receptor D2, downregulated MAOA/MAOB, and ameliorated synaptic injury. MAOB overexpression partially abolished the neuroprotective effect of TMYZD, confirming MAOB as a key target.
CONCLUSIONS: TMYZD improves cognitive function in PSCI by regulating dopamine metabolism, elevating dopamine levels, and enhancing synaptic plasticity, with MAOB as a critical target. These findings provide scientific evidence for the ethnomedical application of TMYZD in PSCI.