Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviate -associated gastritis.
1/5 보강
[BACKGROUND] (HP)-associated gastritis is an important factor in development of stomach cancer.
APA
Li Z, Chen R, et al. (2025). Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviate -associated gastritis.. Histology and histopathology, 40(11), 1847-1857. https://doi.org/10.14670/HH-18-906
MLA
Li Z, et al.. "Sheng-Jiang-Yi-You decoction inhibits the inflammatory response by down-regulating the p38MAPK signaling pathway to alleviate -associated gastritis.." Histology and histopathology, vol. 40, no. 11, 2025, pp. 1847-1857.
PMID
40159952 ↗
Abstract 한글 요약
[BACKGROUND] (HP)-associated gastritis is an important factor in development of stomach cancer. Components of Sheng-Jiang-Yi-You decoction (SJYYD) exert gastroprotective effects. However, the effects and mechanism of SJYYD in HP-associated gastritis remain uncertain.
[METHODS] HP bacterial solution (1×10 CFU/mL) was gavaged every other day for 14 days to construct an HP-associated gastritis mouse model. Male BALB/c mice were randomized into Sham, HP, HP+Standardized triple therapy (HP+Triplet), HP+SJYYD (0.4 mL/20 g), HP+Triplet+SJYYD, HP+anisomycin (ANI) (2.5 mg/kg/d, p38MAPK agonist, HP+ANI), and HP+SJYYD+ANI groups (=6). Gastric mucosal injury detection and rapid urease test for HP infection were conducted. HE staining for pathological damage and ELISA for pro-inflammatory factors and immunoglobulin G (IgG) content were performed. Measurement of p38 mitogen-activated protein kinase (p38MAPK) pathway-related factor expression was performed by qRT-PCR and western blot.
[RESULTS] The increased IgG content and HP colonization rate indicated successful modeling. SJYYD caused attenuated gastric mucosal damage, with decreased ulcer index (UI), HP colonization rate, inflammatory cell infiltration, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β levels in HP-associated gastritis mice. Moreover, SJYYD reduced p38MAPK, c-Jun N-terminal kinase (JNK), and extracellular regulated protein kinase (ERK) mRNA expression, as well as p-p38MAPK/p38MAPK, p-JNK/JNK, and p-ERK/ERK protein expression in gastric mucosa tissues of HP-associated gastritis mice. The above effects were reversed by further ANI treatment.
[CONCLUSION] SJYYD may attenuate HP-associated gastritis by inhibiting inflammatory response by down-regulating p38MAPK pathway, providing scientific evidence for clinical application of SJYYD in HP-associated gastritis treatment and promoting the development of therapeutic approaches in HP-associated gastritis.
[METHODS] HP bacterial solution (1×10 CFU/mL) was gavaged every other day for 14 days to construct an HP-associated gastritis mouse model. Male BALB/c mice were randomized into Sham, HP, HP+Standardized triple therapy (HP+Triplet), HP+SJYYD (0.4 mL/20 g), HP+Triplet+SJYYD, HP+anisomycin (ANI) (2.5 mg/kg/d, p38MAPK agonist, HP+ANI), and HP+SJYYD+ANI groups (=6). Gastric mucosal injury detection and rapid urease test for HP infection were conducted. HE staining for pathological damage and ELISA for pro-inflammatory factors and immunoglobulin G (IgG) content were performed. Measurement of p38 mitogen-activated protein kinase (p38MAPK) pathway-related factor expression was performed by qRT-PCR and western blot.
[RESULTS] The increased IgG content and HP colonization rate indicated successful modeling. SJYYD caused attenuated gastric mucosal damage, with decreased ulcer index (UI), HP colonization rate, inflammatory cell infiltration, tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-1β levels in HP-associated gastritis mice. Moreover, SJYYD reduced p38MAPK, c-Jun N-terminal kinase (JNK), and extracellular regulated protein kinase (ERK) mRNA expression, as well as p-p38MAPK/p38MAPK, p-JNK/JNK, and p-ERK/ERK protein expression in gastric mucosa tissues of HP-associated gastritis mice. The above effects were reversed by further ANI treatment.
[CONCLUSION] SJYYD may attenuate HP-associated gastritis by inhibiting inflammatory response by down-regulating p38MAPK pathway, providing scientific evidence for clinical application of SJYYD in HP-associated gastritis treatment and promoting the development of therapeutic approaches in HP-associated gastritis.
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