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已发表论文
胃和方（Wei-Mi-Shu）通过调节 IL-6/STAT3 信号通路缓解肝胃不和型慢性胃炎
Authors Zou X, Wei M, Jia S, Qi Y, Li H, Liu Y , Li J
Received 25 July 2025
Accepted for publication 26 December 2025
Published 8 January 2026 Volume 2026:19 556234
DOI https://doi.org/10.2147/JIR.S556234
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Dr Alberto Caminero
Xiaoyun Zou,1 Minmin Wei,2 Shouning Jia,3 Yongfu Qi,3 Hailing Li,4 Yan Liu,5 Junru Li6
1Department of Hepatopathy, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China; 2Department of Cardiology, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China; 3Department of Research Institute of Traditional Chinese Medicine, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China; 4Department of Pharmacy, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China; 5Medical College, Qinghai University, Xining, 810016, People’s Republic of China; 6Department of Spleen and Stomach Diseases, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China
Correspondence: Junru Li, Department of Spleen and Stomach Diseases, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China, Email mlqinghai201314@sina.com
Objective: Chronic gastritis, with the liver-stomach disharmony (CG-LSD) type being particularly common, is a prevalent digestive disorder. The Chinese herbal prescription “Wei-Mi-Shu (WMSP)” demonstrated positive therapeutic outcomes in clinical practice for CG-LSD. This study aimed to verify the therapeutic effect of WMSP on CG-LSD and reveal its molecular mechanism based on IL-6/STAT3 pathway.
Methods: Network pharmacology analysis was employed to predict the target genes of WMSP for CG. Following this, a CG-LSD rat model was treated with WMSP, and the changes in body weight, syndrome score, and motor ability were analyzed. The gastric mucosal damage was examined by HE, AB-PAS, and scanning electron microscopy. Serum levels of inflammatory factors and mucosal injury factors were measured via ELISA. Apoptosis was evaluated by TUNEL staining, and the protein expression related to apoptosis and the IL-6/STAT3 pathway was determined by WB. Additionally, a Helicobacter pylori (H. pylori)-infected GES-1 cell model was established to measure cell activity, inflammatory factors levels, and IL-6/STAT3 pathway activation.
Results: Network pharmacology identified 674 common targets between WMSP and CG, including key genes such as TP53, AKT1, TNF, IL-6, and STAT3. In CG-LSD rat models, WMSP significantly improved general health (body weight, symptoms, motor ability), suppressed serum inflammatory factors, and ameliorated gastric mucosal damage (P< 0.05). And it specifically up-regulated the expressions of PG I, GAS17, PGE2, sIgA, and GSH, while down-regulated the expressions of PG II, NOS, ET, GSSG (P< 0.05). Furthermore, WMSP inhibited gastric mucosal cell apoptosis by regulating Bcl-2/Bax (P< 0.05), and suppressed the IL-6/JAK/STAT3 pathway (P< 0.05). In H. pylori-infected GES-1 cell, WMSP enhanced cell viability, and inhibited inflammation and IL-6/JAK/STAT3 activation (P< 0.05). Critically, the protective effects of WMSP on the H. pylori-induced GES-1 cell were inhibited by a STAT3 activator (P< 0.05).
Conclusion: WMSP alleviated inflammation, apoptosis, and mucosal injury in CG-LSD by targeting the IL-6/STAT3 axis.
Keywords: Wei-Mi-Shu prescription, chronic gastritis with liver- stomach disharmony, inflammatory response, IL-6/STAT3 pathway
1Department of Hepatopathy, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China; 2Department of Cardiology, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China; 3Department of Research Institute of Traditional Chinese Medicine, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China; 4Department of Pharmacy, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China; 5Medical College, Qinghai University, Xining, 810016, People’s Republic of China; 6Department of Spleen and Stomach Diseases, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China
Correspondence: Junru Li, Department of Spleen and Stomach Diseases, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining, 810000, People’s Republic of China, Email mlqinghai201314@sina.com
Objective: Chronic gastritis, with the liver-stomach disharmony (CG-LSD) type being particularly common, is a prevalent digestive disorder. The Chinese herbal prescription “Wei-Mi-Shu (WMSP)” demonstrated positive therapeutic outcomes in clinical practice for CG-LSD. This study aimed to verify the therapeutic effect of WMSP on CG-LSD and reveal its molecular mechanism based on IL-6/STAT3 pathway.
Methods: Network pharmacology analysis was employed to predict the target genes of WMSP for CG. Following this, a CG-LSD rat model was treated with WMSP, and the changes in body weight, syndrome score, and motor ability were analyzed. The gastric mucosal damage was examined by HE, AB-PAS, and scanning electron microscopy. Serum levels of inflammatory factors and mucosal injury factors were measured via ELISA. Apoptosis was evaluated by TUNEL staining, and the protein expression related to apoptosis and the IL-6/STAT3 pathway was determined by WB. Additionally, a Helicobacter pylori (H. pylori)-infected GES-1 cell model was established to measure cell activity, inflammatory factors levels, and IL-6/STAT3 pathway activation.
Results: Network pharmacology identified 674 common targets between WMSP and CG, including key genes such as TP53, AKT1, TNF, IL-6, and STAT3. In CG-LSD rat models, WMSP significantly improved general health (body weight, symptoms, motor ability), suppressed serum inflammatory factors, and ameliorated gastric mucosal damage (P< 0.05). And it specifically up-regulated the expressions of PG I, GAS17, PGE2, sIgA, and GSH, while down-regulated the expressions of PG II, NOS, ET, GSSG (P< 0.05). Furthermore, WMSP inhibited gastric mucosal cell apoptosis by regulating Bcl-2/Bax (P< 0.05), and suppressed the IL-6/JAK/STAT3 pathway (P< 0.05). In H. pylori-infected GES-1 cell, WMSP enhanced cell viability, and inhibited inflammation and IL-6/JAK/STAT3 activation (P< 0.05). Critically, the protective effects of WMSP on the H. pylori-induced GES-1 cell were inhibited by a STAT3 activator (P< 0.05).
Conclusion: WMSP alleviated inflammation, apoptosis, and mucosal injury in CG-LSD by targeting the IL-6/STAT3 axis.
Keywords: Wei-Mi-Shu prescription, chronic gastritis with liver- stomach disharmony, inflammatory response, IL-6/STAT3 pathway