Journal of ethnopharmacology · 2025
Puerariae Lobatae Radix-Gastrodiae Rhizoma ameliorates nitroglycerin-induced chronic migraine by modulating p38 MAPK/CREB signaling pathway in the prefrontal cortex-thalamus neural circuit.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Wang Zhujun, Zhu Tingting, Ren Keke, Ouyang Hui, Pan Qihong, Feng Yuling, Yang Shiling
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Puerariae Lobatae Radix (PLR) and Gastrodiae Rhizoma (GR) are classic "medicine-food homology" pairs in Traditional Chinese Medicine (TCM). For millennia, they have been used in formulas to treat headache and vertigo, as recorded in Compendium of Materia Medica and Shennong's Classic of Materia Medica. Clinical practices confirm their efficacy in alleviating migraine, but the underlying mechanisms remain unclear.
AIM OF THE STUDY: This study aimed to evaluate the therapeutic effect of PLR-GR on chronic migraine and elucidate its potential mechanism of improving migraine the perspective of neural regulation, focusing on the p38 MAPK/CREB signaling pathway in the prefrontal cortical-thalamus (PFC-THAL) neural circuit.
MATERIALS AND METHODS: A chronic migraine model was constructed in SD female rat, and the effects of PLR-GR on migraine were examined using enzyme-linked immunosorbent assay, real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), histopathological staining (HE) and immunofluorescence (IF) analysis. Comprehensive analyses including non-targeted metabolomics, spatial metabolomics, transcriptomics, and western blotting were utilized to study the molecular mechanism of PLR-GR protecting neuronal cells and improving migraine.
RESULTS: PLR-GR can regulate weight, pain threshold and the contents of CGRP, iNOS, NO, ET, 5-HT in the plasma of migraine rats, reduce the levels of inflammatory factors IL-6, TNF-α, PG-E2 in brain tissue, protect the neuronal cells in the prefrontal cortex (PFC) and thalamus (THAL), and alleviates the pathological damage of the brain 's nervous system. Non-targeted metabolomic analysis revealed PLR-GR reversed 52 differential plasma metabolites (e.g., tauroursodeoxycholic acid, SM (d18: 1/17: 0)), involving sphingolipid and bile acid metabolism. Spatial metabolomics showed it normalized neurotransmitters (glutamate, GABA) and lipids (PE, PG) in PFC-THAL. Transcriptomics identified 176 differential genes regulated by PLR-GR, enriched in calcium signaling and cAMP pathways. Integrated multi-omics and Western blot confirmed PLR-GR could down-regulate the protein phosphorylation expression of p38 MAPK/CREB signaling pathway in the neural circuit.
CONCLUSION: This study is the first to focus on the role of PFC-THA circuits in migraine and reveal the molecular mechanism by which PLR-GR can alleviate migraine damage by regulating metabolic network and neurotransmitter levels.
AIM OF THE STUDY: This study aimed to evaluate the therapeutic effect of PLR-GR on chronic migraine and elucidate its potential mechanism of improving migraine the perspective of neural regulation, focusing on the p38 MAPK/CREB signaling pathway in the prefrontal cortical-thalamus (PFC-THAL) neural circuit.
MATERIALS AND METHODS: A chronic migraine model was constructed in SD female rat, and the effects of PLR-GR on migraine were examined using enzyme-linked immunosorbent assay, real-time fluorescence quantitative polymerase chain reaction (RT-qPCR), histopathological staining (HE) and immunofluorescence (IF) analysis. Comprehensive analyses including non-targeted metabolomics, spatial metabolomics, transcriptomics, and western blotting were utilized to study the molecular mechanism of PLR-GR protecting neuronal cells and improving migraine.
RESULTS: PLR-GR can regulate weight, pain threshold and the contents of CGRP, iNOS, NO, ET, 5-HT in the plasma of migraine rats, reduce the levels of inflammatory factors IL-6, TNF-α, PG-E2 in brain tissue, protect the neuronal cells in the prefrontal cortex (PFC) and thalamus (THAL), and alleviates the pathological damage of the brain 's nervous system. Non-targeted metabolomic analysis revealed PLR-GR reversed 52 differential plasma metabolites (e.g., tauroursodeoxycholic acid, SM (d18: 1/17: 0)), involving sphingolipid and bile acid metabolism. Spatial metabolomics showed it normalized neurotransmitters (glutamate, GABA) and lipids (PE, PG) in PFC-THAL. Transcriptomics identified 176 differential genes regulated by PLR-GR, enriched in calcium signaling and cAMP pathways. Integrated multi-omics and Western blot confirmed PLR-GR could down-regulate the protein phosphorylation expression of p38 MAPK/CREB signaling pathway in the neural circuit.
CONCLUSION: This study is the first to focus on the role of PFC-THA circuits in migraine and reveal the molecular mechanism by which PLR-GR can alleviate migraine damage by regulating metabolic network and neurotransmitter levels.