Weimishu prescription (胃糜舒方) alleviates liver-stomach disharmony and chronic gastritis by reducing inflammation and regulating gastric stem cell differentiation

doi:10.19852/j.cnki.jtcm.2026.01.009

Journal of Traditional Chinese Medicine ›› 2026, Vol. 46 ›› Issue (1): 95-109.DOI: 10.19852/j.cnki.jtcm.2026.01.009

• Original Articles • Previous Articles Next Articles

Weimishu prescription (胃糜舒方) alleviates liver-stomach disharmony and chronic gastritis by reducing inflammation and regulating gastric stem cell differentiation

ZOU Xiaoyun¹^,², WEI Minmin³, JIA Shouning⁴, QI Yongfu⁴, LI Hailing⁵, LIU Yan¹, SHI Xiujuan¹, LI Junru⁶()

1 Medical colledge, Qinghai University, Xining 810016, China
2 Department of Hepatopathy, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining 810000, China
3 Department of Cardiology, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining 810000, China
4 Department of Reserch Institute of Traditional Chinese Medicine, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining 810000, China
5 Department of Pharmacy, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining 810000, China
6 Department of Spleen and Stomach Diseases, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining 810000, China

Received:2025-04-14 Accepted:2025-11-20 Online:2026-02-15 Published:2026-01-28
Contact: Pro. LI Junru, Department of Spleen and Stomach Diseases, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining 810000, China. mlqinghai201314@sina.com;Telephone: +86-13519732841
About author:Pro. LI Junru, Department of Spleen and Stomach Diseases, Qinghai Provincial Hospital of Traditional Chinese Medicine, Xining 810000, China. mlqinghai201314@sina.com;Telephone: +86-13519732841
Supported by:
2023 Traditional Chinese Medicine Innovation Capability Enhancement Project from the National Administration of Traditional Chinese Medicine(no number);2024 Qinghai Province “Kunlun Talents ? High-End Innovative and Entrepreneurial Talents” Top Notch Talent Project(QHKLYC-GDCXCY-2024-152);Study the Mechanism of Weimishu Prescription in the Treatment of Chronic Gastritis with Liver-Stomach Disharmony

Abstract

Abstract:

OBJECTIVE: To investigate the therapeutic effect of Weimishu prescription (胃糜舒方, WMSP) on chronic gastritis with liver-stomach disharmony (CG-LSD) and elucidate its molecular mechanisms involved in regulating the nuclear factor kappa-B (NF-κB) inflammatory response and gastric stem cell (GSC) differentiation.

METHODS: A CG-LSD rat model was established through a combined protocol involving 56% ethanol and tail-clip stimulation. Rats were administered with low-, medium-, or high-dose WMSP, the positive control drug omeprazole, or high-dose WMSP with the NF-κB agonist phorbol 12-myristate 13-acetate (PMA). Histopathological changes were assessed via hematoxylin and eosin and TdT-mediated dUTP nick end labeling staining. Flow cytometry, immunofluorescence, real-time quantitative polymerase chain reaction, Western blotting, and enzyme-linked immunosorbent assay were performed to evaluate the underlying mechanisms.

RESULTS: WMSP significantly increased rat locomotor activity, improved Traditional Chinese Medicine syndrome scores, and ameliorated pathological damage to the gastric mucosa while reducing gastric mucosal epithelial cells apoptosis. WMSP also increased the proportion of Lgr5⁺Ki67⁺ cells; upregulated muscle, intestine, and stomach specific transcript 1, sex determining region Y-box 2, sex determining region Y-box 9, and homing cell adhesion molecule; and enhanced the levels of pepsinogen C, somatostatin, mucin-6, H⁺-K⁺ATPase, and E-cadherin proteins, thereby promoting gastric stem cell survival and differentiation. Furthermore, WMSP alleviated systemic and gastric mucosal inflammation in CG-LSD rats. Mechanistically, WMSP suppressed NF-κB expression, thereby reducing Smad-specific E3 ubiquitin ligase 2 levels, which enhanced β-catenin and subsequently increased myelocytomatosis oncogene, and axis inhibition protein 2 expression. PMA administration reversed the protective effect of WMSP on CG-LSD rats.

CONCLUSIONS: WMSP ameliorated gastric mucosal injury in CG-LSD rats by regulating the NF-κB/β-catenin signaling pathway, thereby suppressing inflammation and promoting gastric stem cell differentiation. These findings highlight the therapeutic potential of WMSP, providing the foundation for further clinical evaluations of WMSP in CG-LSD treatment.

Key words: gastritis, liver-stomach disharmony, NF-kappa B, inflammation, Weimishu prescription

ZOU Xiaoyun, WEI Minmin, JIA Shouning, QI Yongfu, LI Hailing, LIU Yan, SHI Xiujuan, LI Junru. Weimishu prescription (胃糜舒方) alleviates liver-stomach disharmony and chronic gastritis by reducing inflammation and regulating gastric stem cell differentiation[J]. Journal of Traditional Chinese Medicine, 2026, 46(1): 95-109.

Figures/Tables 9

Figure 1 WMSP improved the liver-stomach disharmony syndrome in CG-LSD rats A: Traditional Chinese Medicine syndrome scores of CG-LSD rats based on emotional condition, hair condition, stool condition, and food intake (n = 6); B: moving distance of rats in OFT (n = 3); C: representative images of OFT; C1: control group; C2: model group; C3: OME group; C4: WMSP-L group; C5: WMSP-M group; C6: WMSP-H group; C7: WMSP-H + PMA group. Control group: normal rats without CG-LSD model or treatment; Model group: rats with CG-LSD, without treatment; OME group: CG-LSD rats treated with positive drug omeprazole (20 mg/kg); WMSP-L group: CG-LSD rats treated with low-dose WMSP (8.7 g·kg?1·d?1); WMSP-M group: CG-LSD rats treated with middle-dose WMSP (17.3 g·kg?1·d?1); WMSP-H group: CG-LSD rats treated with high-dose WMSP (34.6 g·kg?1·d?1); WMSP-H+PMA group: CG-LSD rats treated with high-dose WMSP (34.6 g·kg?1·d?1) and NF-κB agonist PMA (20 ng·kg?1·d?1). CG-LSD: chronic gastritis with liver-stomach disharmony; OFT: open field test; OME: omeprazole; WMSP: Weimishu prescription; PMA: phorbol 12-myristate 13-acetate; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by post hoc testing. Data were presented as the mean ± standard deviation. aP < 0.01 vs the control group; bP < 0.01 vs the model group; cP < 0.05, dP < 0.01 vs the WMSP-H group.

Table 1 Body weight of rats (g, $\bar{x} \pm s$)

Week	Control (n = 6)	Model (n = 6)	OME (n = 5)	WMSP-L (n = 6)	WMSP-M (n = 6)	WMSP-H (n = 5)	WMSP-H+PMA (n = 6)
0	225±3	222±3	225±6	225±5	220±4	224±4	222±5
1	307±8	303±12	297±16	295±9	295±12	302±7	296±12
2	379±23	359±18	356±18	357±19	357±28	360±18	358±22
3	451±12	403±17^a	404±15	405±24	409±33	407±21	403±16
4	502±18	451±17^b	454±16	460±24	451±49	460±26	443±31
5	529±18	474±19^b	480±12	478±31	480±48	479±17	476±22
6	554±16	490±29^b	492±29	496±31	494±45	494±19	491±19
7	605±23	507±18^b	505±23	509±38	511±39	509±17	509±26
8	624±28	516±20^b	558±36	542±27	552±41	562±13	536±22
9	632±44	524±17^b	586±40^c	554±29	565±44	580±25	548±35
10	646±33	535±14^b	603±29^c	576±23	584±44^d	596±20^d	563±43
11	655±32	529±31^b	625±26^c	589±24^c	602±45^c	614±17^c	572±44

Figure 2 WMSP improves gastric mucosa injury in CG-LSD rats A1-A7: representative images of HE staining of gastric mucosal tissues (magnification = × 100), scare bar = 200 μm; A8-A14: representative images of HE staining of gastric mucosal tissues (magnification = × 400), scare bar = 50 μm. A1, A8: control group; A2, A9: model group; A3, A10: OME group; A4, A11: WMSP-L group; A5, A12: WMSP-M group; A6, A13: WMSP-H group; A7, A14: WMSP-H + PMA group; B: representative images of TUNEL staining. Scare bar = 20 μm. B1-B7: DAPI stained gastric mucosal epithelial cells in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; B8-B14: TUNEL stained gastric mucosal epithelial cells in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; B15-B21: merge of DAPI and TUNEL stained gastric mucosal epithelial cells in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; C: histopathological scores of HE staining, characterized by mucosal cell atrophy, necrosis, and decline; inflammatory cell infiltration; hemorrhage; and fibrous tissue proliferation; D: the apoptosis rate of gastric mucosal epithelial cells. Control group: normal rats without CG-LSD model or treatment; Model group: rats with CG-LSD, without treatment; OME group: CG-LSD rats treated with positive drug omeprazole (20 mg/kg); WMSP-L group: CG-LSD rats treated with low-dose WMSP (8.7 g·kg?1·d?1); WMSP-M group: CG-LSD rats treated with middle-dose WMSP (17.3 g·kg?1·d?1); WMSP-H group: CG-LSD rats treated with high-dose WMSP (34.6 g·kg?1·d?1); WMSP-H + PMA group: CG-LSD rats treated with high-dose WMSP (34.6 g·kg?1·d?1) and NF-κB agonist PMA (20 ng·kg?1·d?1). CG-LSD: chronic gastritis with liver-stomach disharmony; OME: omeprazole; WMSP: Weimishu prescription; PMA: phorbol 12-myristate 13-acetate; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by post hoc testing. Data were presented as the mean ± standard deviation (n = 3). aP < 0.01 vs the control group; bP < 0.01, cP < 0.05, vs the model group; dP < 0.01 vs the WMSP-H group.

Figure 3 WMSP promoted the survival and differentiation of gastric stem cells (GSCs) in CG-LSD rats A: representative images of flow cytometry. A1: control group; A2: model group; A3: OME group; A4: WMSP-L group; A5: WMSP-M group; A6: WMSP-H group; A7: WMSP-H + PMA group; B: the percentage of Lgr5+Ki67+ cells in gastric tissue detected by flow cytometry; C: representative images of immunofluorescence staining, scare bar = 50 μm; C1-C7: DAPI stained GSCs in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; C8-C14: Lgr5 stained GSCs in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; C15-C21: merge of DAPI and Lgr5 stained GSCs in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; D: immunofluorescence staining results indicating the number of Lgr5-positive cells; E: the expression levels of the main cell marker (PGC), endocrine cell marker (SST), gastric gland mucous cell marker (MUC6), parietal cell marker (H+-K+ATP4B), and epithelial cell marker (E-cadherin) proteins detected by Western blot. Control group: normal rats without CG-LSD model or treatment; Model group: rats with CG-LSD, without treatment; OME group: CG-LSD rats treated with positive drug omeprazole (20 mg/kg); WMSP-L group: CG-LSD rats treated with low-dose WMSP (8.7 g·kg?1·d?1); WMSP-M group: CG-LSD rats treated with middle-dose WMSP (17.3 g·kg?1·d?1); WMSP-H group: CG-LSD rats treated with high-dose WMSP (34.6 g·kg?1·d?1); WMSP-H + PMA group: CG-LSD rats treated with high-dose WMSP (34.6 g·kg?1·d?1) and NF-κB agonist PMA (20 ng·kg?1·d?1). CG-LSD: chronic gastritis with liver-stomach disharmony; OME: omeprazole; WMSP: Weimishu prescription; PMA: phorbol 12-myristate 13-acetate; Lgr5: leucine-rich repeat-containing G protein-coupled receptor 5; GSCs: gastric stem cells; MUC6: mucin-6; PGC: pepsinogen C; SST: somatostatin; H+-K+ATP4B: hydrogen potassium ATPase beta; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by post hoc testing. Data are presented as the mean ± standard deviation (n = 3). aP < 0.01 vs the control group; bP < 0.01 vs the model group; cP < 0.01 vs the WMSP-H group.

Table 2 GSCs-related markers (Mist1, Sox2, SOX9, and CD44) mRNA expression (2－△△CT) detected using RT-qPCR ($\bar{x} \pm s$)

Group	n	Mist1	SOX2	SOX9	CD44
Control	3	1.033±0.305	1.017±0.230	1.03±0.31	1.013±0.222
Model	3	0.243±0.032^a	0.203±0.025^a	0.22±0.01^a	0.147±0.015^a
OME	3	0.813±0.227^b	0.837±0.206^b	0.90±0.25^b	0.850±0.182^b
WMSP-L	3	0.517±0.137	0.437±0.117	0.48±0.15	0.343±0.130
WMSP-M	3	0.630±0.135^c	0.533±0.143^c	0.58±0.07^c	0.557±0.146^b
WMSP-H	3	0.723±0.112^b	0.703±0.188^b	0.71±0.26^b	0.703±0.222^b
WMSP-H+PMA	3	0.393±0.091^d	0.313±0.050^e	0.35±0.08^d	0.253±0.045^e

Table 3 Western blot assay for quantitative analysis of PGC, SST, MUC6, H + -K + ATP4B, and E-cadherin proteins ($\bar{x} \pm s$)

Group	n	MUC6	PGC	SST	ATP4B	E-cadherin
Control	3	1.000±0.048	1.000±0.046	1.000±0.054	1.006±0.117	1.001±0.058
Model	3	0.137±0.061^a	0.329±0.015^a	0.086±0.036^a	0.114±0.013^a	0.155±0.017^a
OME	3	0.775±0.060^b	0.711±0.060^b	0.836±0.088^b	0.850±0.066^b	0.772±0.028^b
WMSP-L	3	0.528±0.080^b	0.565±0.057^b	0.496±0.049^b	0.291±0.032^b	0.425±0.034^b
WMSP-M	3	0.637±0.114^b	0.615±0.063^b	0.663±0.049^b	0.400±0.081^b	0.537±0.021^b
WMSP-H	3	0.814±0.062^b	0.695±0.018^b	0.832±0.084^b	0.735±0.065^b	0.785±0.066^b
WMSP-H+PMA	3	0.336±0.053^c	0.412±0.029^c	0.151±0.024^c	0.146±0.033^c	0.277±0.039^c

Table 4 Levels of inflammatory factors in the serum and gastric mucosal tissues of rats (pg/mL, $\bar{x} \pm s$)

Group	n	Serum				Gastric mucosa
Group	n	IL-1β	IL-6	IL-17	TNF-α		IL-1β	IL-6	IL-17	TNF-α
Control	3	3.4±0.7	19.4±3.8	5.2±0.3	28.9±3.1	2.0±0.6		14.8±3.7	2.9±0.4	16.3±2.2
Model	3	8.6±0.7^a	35.4±4.1^a	8.1±0.5^a	59.0±4.3^a	6.3±0.6^a		36.0±4.6^a	6.7±0.4^a	40.9±2.7^a
OME	3	5.9±1.0^b	25.9±2.9^b	6.5±0.8^b	37.8±3.5^b	3.8±0.8^b		20.6±3.6^b	4.3±0.7^b	19.4±5.7^b
WMSP-L	3	7.2±0.5^c	29.7±2.5^c	7.1±0.7^c	50.5±5.3^c	5.1±0.7^c		29.5±1.6^c	5.4±0.6^c	32.1±4.9^c
WMSP-M	3	6.0±1.0^b	26.5±2.5^b	6.7±0.5^c	44.9±4.8^b	4.3±0.6^b		23.6±2.2^b	4.7±0.9^c	26.1±5.3^b
WMSP-H	3	5.3±0.7^b	23.6±2.7^b	5.7±0.7^b	41.0±4.6^b	3.8±0.5^b		16.5±1.4^b	4.1±0.7^b	20.4±3.6^b
WMSP-H+PMA	3	7.8±0.7^d	31.3±3.1^d	7.3±0.4^d	53.9±3.7^d	5.8±0.7^d		33.3±3.0^d	6.1±0.6^d	35.2±2.7^d

Figure 4 WMSP regulated the NF-κB/β-catenin pathway in CG-LSD rats A: Western blotting used to detect the expression of IκBα, p-IκBα, Smurf2, and β-catenin in gastric mucosal tissues; B: quantitative data of NF-κB p65-positive cells in the nucleus; C: immunofluorescence staining used to detect the nuclear localization of NF-κB p65. Scare bar = 50 μm. C1-C7: DAPI stained GSCs in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; C8-C14: Lgr5 stained GSCs in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; C15-C21: merge of DAPI and Lgr5 stained GSCs in the control, model, OME, WMSP-L, WMSP-M, WMSP-H, and WMSP-H + PMA groups; D: RT-qPCR performed to measure the expression levels of c-MYC in gastric mucosal tissues; E: RT-qPCR performed to measure the expression levels of AXIN2 in gastric mucosal tissues. Control group: normal rats without CG-LSD model or treatment; Model group: rats with CG-LSD, without treatment; OME group: CG-LSD rats treated with positive drug omeprazole (20 mg/kg); WMSP-L group: CG-LSD rats treated with low-dose WMSP (8.7 g·kg?1·d?1); WMSP-M group: CG-LSD rats treated with middle-dose WMSP (17.3 g·kg?1·d?1); WMSP-H group: CG-LSD rats treated with high-dose WMSP (34.6 g·kg?1·d?1); WMSP-H + PMA group: CG-LSD rats treated with high-dose WMSP (34.6 g·kg?1·d?1) and NF-κB agonist PMA (20 ng·kg?1·d?1). CG-LSD: chronic gastritis with liver-stomach disharmony; OME: omeprazole; WMSP: Weimishu prescription; PMA: phorbol 12-myristate 13-acetate; SMURF2: Smad-specific E3 ubiquitin ligase 2; IkBα: I-kappa-B-alpha; c-MYC: myelocytomatosis oncogene; AXIN2: axis inhibition protein 2; RT-qPCR: real-time quantitative polymerase chain reaction; ANOVA: analysis of variance. Statistical analysis was performed using one-way ANOVA followed by post hoc testing. Data are presented as the mean ± standard deviation (n = 3). aP < 0.01 vs the control group; bP < 0.01, cP < 0.05 vs the model group; dP < 0.01 vs the WMSP-H group.

Table 5 Quantitative analysis of the NF-κB/β-catenin pathway proteins via Western blotting

Group	n	SMURF2	IκBα	p-IκBα	β-catenin
Control	3	1.01±0.13	1.00±0.12	1.00±0.04	1.01±0.12
Model	3	2.71±0.13^a	1.15±0.11^a	6.08±0.29^a	0.23±0.06^a
OME	3	1.53±0.04^b	1.07±0.04	3.12±0.20^b	0.81±0.05^b
WMSP-L	3	2.02±0.09^b	1.07±0.04	4.84±0.12^b	0.58±0.04^b
WMSP-M	3	1.83±0.14^b	1.08±0.07	4.33±0.31^b	0.70±0.04^b
WMSP-H	3	1.51±0.09^b	1.05±0.14	3.23±0.15^b	0.86±0.07^b
WMSP-H+PMA	3	2.15±0.09^c	1.08±0.06	5.31±0.06^c	0.49±0.13^c

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Weimishu prescription (胃糜舒方) alleviates liver-stomach disharmony and chronic gastritis by reducing inflammation and regulating gastric stem cell differentiation

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