Journal of ethnopharmacology · 2026
Xiongzhi Qufeng Zhitong Granule alleviates nitroglycerin-induced migraine-like nociception and central neuroinflammation by regulating the HMGB1 / TRPV1 / MAPK signaling axis.
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Huang Lianzhan, Zhou Jieru, Han Yiyue, Mou Xiaotong, Zheng Yixin, Liu Changjiang, Ou Yanghan, Ding Xuansheng, Han Bing
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Chronic migraine (CM) represents a highly prevalent neuroinflammatory disorder with limited therapeutic options. Xiongzhi Qufeng Zhitong Granules (XZQF), a clinically used traditional Chinese medicine, displays promising anti-migraine potential with favorable safety profiles; however, its systematic efficacy and underlying mechanisms remain poorly defined.
AIM OF THE STUDY: This study aimed to investigate the protective effects of XZQF on a CM model in rats triggered by nitroglycerin (NTG) injection, and to unveil the potential mechanisms focusing on HMGB1/TRPV1/MAPK signaling pathway.
MATERIALS AND METHODS: A CM rat model was first established, and the effects of XZQF on CM were evaluated integrating behavioral testing, enzyme-linked immunosorbent assay (ELISA), and histopathological staining analysis. Subsequently, anti-CM mechanism verification, including network pharmacological analysis, immunofluorescence, immunohistochemistry, and Western blotting, were employed to reveal the molecular mechanism of XZQF in regulating HMGB1/TRPV1/MAPK signaling axis to against CM.
RESULTS: Both behavioral assays, ELISA test, and histopathological assessment demonstrated that XZQF significantly restored body weight and pain thresholds, reduced serum and brain levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), pain modulators (PGE2, 5-HT, β-EP), and vasoactive mediators (CGRP, VIP, NO, iNOS), while alleviating migraine-associated brain tissue damage. Network pharmacology identified core targets (STAT3, NFKB1, JUN, PTGS2, IL1B) and key bioactive components (ferulic acid, senkyunolides E/F, neocnidilide, methyleugenol), with enrichment in MAPK, PI3K-Akt, and cAMP signaling cascades. Immunofluorescence, immunohistochemistry, and Western blotting further validated that XZQF markedly suppressed the expression of CGRP, TRPV1, c-Fos, COX-2, and HMGB1, as well as the phosphorylation of MEK and MAPK.
CONCLUSION: Collectively, these findings demonstrate that XZQF exerts robust analgesic, anti-inflammatory, and vasoregulatory effects against CM by blunting central neuroinflammation through the HMGB1/TRPV1/MAPK signaling axis. Our work establishes a mechanistic framework for understanding the anti-CM activity of XZQF and supports its further development as a therapeutic intervention for CM.
AIM OF THE STUDY: This study aimed to investigate the protective effects of XZQF on a CM model in rats triggered by nitroglycerin (NTG) injection, and to unveil the potential mechanisms focusing on HMGB1/TRPV1/MAPK signaling pathway.
MATERIALS AND METHODS: A CM rat model was first established, and the effects of XZQF on CM were evaluated integrating behavioral testing, enzyme-linked immunosorbent assay (ELISA), and histopathological staining analysis. Subsequently, anti-CM mechanism verification, including network pharmacological analysis, immunofluorescence, immunohistochemistry, and Western blotting, were employed to reveal the molecular mechanism of XZQF in regulating HMGB1/TRPV1/MAPK signaling axis to against CM.
RESULTS: Both behavioral assays, ELISA test, and histopathological assessment demonstrated that XZQF significantly restored body weight and pain thresholds, reduced serum and brain levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α), pain modulators (PGE2, 5-HT, β-EP), and vasoactive mediators (CGRP, VIP, NO, iNOS), while alleviating migraine-associated brain tissue damage. Network pharmacology identified core targets (STAT3, NFKB1, JUN, PTGS2, IL1B) and key bioactive components (ferulic acid, senkyunolides E/F, neocnidilide, methyleugenol), with enrichment in MAPK, PI3K-Akt, and cAMP signaling cascades. Immunofluorescence, immunohistochemistry, and Western blotting further validated that XZQF markedly suppressed the expression of CGRP, TRPV1, c-Fos, COX-2, and HMGB1, as well as the phosphorylation of MEK and MAPK.
CONCLUSION: Collectively, these findings demonstrate that XZQF exerts robust analgesic, anti-inflammatory, and vasoregulatory effects against CM by blunting central neuroinflammation through the HMGB1/TRPV1/MAPK signaling axis. Our work establishes a mechanistic framework for understanding the anti-CM activity of XZQF and supports its further development as a therapeutic intervention for CM.