Journal of ethnopharmacology · 2026
Shisanwei Qinglan Powder attenuates ethanol-induced gastric mucosal injury in association with reduced NF-κB signalling and caspase activation.
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Ye Kanshen, Li Haoqin, Qin Zhizheng, Zhu Zichen, Wang Rui, Dou Jie, Ren Qingjia, Liu Xiaoya, Wang Fei
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Shisanwei Qinglan Powder (SQP) is a marketed Tibetan medicinal formula traditionally used for gastrointestinal disorders associated with "peigen mubu", including epigastric distension and pain, gastritis, and ulcer-related symptoms. However, experimental evidence for the complete formula, its systemically exposed constituents, and the mechanisms underlying gastric mucosal protection remains limited.
AIM OF THE STUDY: This study aimed to characterise the serum-associated constituents of SQP and evaluate its protective effects and molecular responses in acute ethanol-induced gastric mucosal injury.
MATERIALS AND METHODS: Chemical profiling and serum pharmacochemistry were performed by liquid chromatography-tandem mass spectrometry. Network pharmacology and gastric-tissue transcriptomics were integrated to prioritise treatment-associated pathways. Pharmacological effects were evaluated in mice receiving SQP prophylactically before anhydrous ethanol challenge and in GES-1 cells receiving SQP after ethanol-induced injury, using viability, migration, apoptosis, macroscopic lesion, histological, oxidative-stress, and inflammatory measurements. The IKKβ/IκBα/NF-κB axis and caspase-8/caspase-3 activation were assessed by immunohistochemistry and western blotting. Selected compound-target pairs were further evaluated by molecular docking and 100-ns molecular dynamics simulations.
RESULTS: Thirty-two distinct serum-associated constituents were tentatively identified, and 185 targets were shared between SQP- and gastric ulcer-related datasets. Under the post-injury cell-intervention paradigm, SQP improved viability and migration, corrected oxidative and cytokine imbalances, and reduced total apoptosis from approximately 21.9% to 7.9% at 20 μg/mL. Under the prophylactic animal paradigm, SQP alleviated haemorrhage, erosion, and glandular disruption, and 0.52 g/kg significantly reduced both the ulcer index and damaged area. RNA sequencing identified 1,533 differentially expressed genes between the high-dose SQP and model groups, with enrichment in TNF, NF-κB and apoptosis-related pathways. In both models, SQP reduced phosphorylation of IKKβ, IκBα and NF-κB p65, suppressed caspase-8 and caspase-3 cleavage, and decreased gastric TUNEL positivity. Molecular docking and molecular dynamics simulations were used for computational prioritization of the TNF-bicuculline and CASP3-kaempferol pairs; these analyses indicated structural feasibility under the simulated conditions but did not establish direct binding or target engagement.
CONCLUSION: SQP showed prophylactic gastroprote ctive effects in mice and post-injury protective and reparative effects in ethanol-injured GES-1 cells. Across these distinct experimental paradigms, the observed effects were associated with attenuation of oxidative stress, IKK/NF-κB-related inflammation, and caspase-8/caspase-3-associated apoptotic responses.
AIM OF THE STUDY: This study aimed to characterise the serum-associated constituents of SQP and evaluate its protective effects and molecular responses in acute ethanol-induced gastric mucosal injury.
MATERIALS AND METHODS: Chemical profiling and serum pharmacochemistry were performed by liquid chromatography-tandem mass spectrometry. Network pharmacology and gastric-tissue transcriptomics were integrated to prioritise treatment-associated pathways. Pharmacological effects were evaluated in mice receiving SQP prophylactically before anhydrous ethanol challenge and in GES-1 cells receiving SQP after ethanol-induced injury, using viability, migration, apoptosis, macroscopic lesion, histological, oxidative-stress, and inflammatory measurements. The IKKβ/IκBα/NF-κB axis and caspase-8/caspase-3 activation were assessed by immunohistochemistry and western blotting. Selected compound-target pairs were further evaluated by molecular docking and 100-ns molecular dynamics simulations.
RESULTS: Thirty-two distinct serum-associated constituents were tentatively identified, and 185 targets were shared between SQP- and gastric ulcer-related datasets. Under the post-injury cell-intervention paradigm, SQP improved viability and migration, corrected oxidative and cytokine imbalances, and reduced total apoptosis from approximately 21.9% to 7.9% at 20 μg/mL. Under the prophylactic animal paradigm, SQP alleviated haemorrhage, erosion, and glandular disruption, and 0.52 g/kg significantly reduced both the ulcer index and damaged area. RNA sequencing identified 1,533 differentially expressed genes between the high-dose SQP and model groups, with enrichment in TNF, NF-κB and apoptosis-related pathways. In both models, SQP reduced phosphorylation of IKKβ, IκBα and NF-κB p65, suppressed caspase-8 and caspase-3 cleavage, and decreased gastric TUNEL positivity. Molecular docking and molecular dynamics simulations were used for computational prioritization of the TNF-bicuculline and CASP3-kaempferol pairs; these analyses indicated structural feasibility under the simulated conditions but did not establish direct binding or target engagement.
CONCLUSION: SQP showed prophylactic gastroprote ctive effects in mice and post-injury protective and reparative effects in ethanol-injured GES-1 cells. Across these distinct experimental paradigms, the observed effects were associated with attenuation of oxidative stress, IKK/NF-κB-related inflammation, and caspase-8/caspase-3-associated apoptotic responses.