Naeso-san, a traditional herbal formula, attenuates HCl/ethanol-induced gastric ...

연구 요약

Naeso-san, a traditional herbal formula, attenuates HCl/ethanol-induced gastric injury via MAPK and NF-κB pathway modulation in mice.

Frontiers in pharmacology 학술지에 발표된 이 연구는 Choi S, Ju IG, Lee M 외 연구팀이 수행하였습니다.

이 연구는 'Naeso-san, a traditional herbal formula, attenuates HCl/ethanol-induced gastric injury via MAPK and NF-κB pathway modulation in mice.'에 대한 과학적 분석을 제공합니다.

핵심 내용

BACKGROUND: Gastric ulcers affect approximately 10% of the global population, while current acid-suppressive therapies have notable limitations including impaired digestion and long-term safety concerns. Naeso-san (NSS), a traditional botanical formulation, has shown promising gastroprotective effects, yet its precise molecular mechanisms remain incompletely understood. This study investigated the molecular pathways underlying its gastroprotective effects versus conventional therapies. METHODS: We evaluated the gastroprotective effects of NSS (75, 300, 1200 mg/kg) in 7-week-old male ICR mice using a hydrochloric acid/ethanol (HCl/EtOH)-induced gastric injury model, with ranitidine (40 mg/kg) as positive control. Macroscopic damage scores were assessed, and molecular mechanisms including pro-inflammatory cytokines and mitogen-activated protein kinase (MAPK), protein kinase B (AKT), and nuclear factor-κB (NF-κB) signaling pathways were analyzed. In vitro studies using TNF-α-stimulated human gastric adenocarcinoma cell line (MKN45) gastric epithelial cells assessed inflammatory gene expression and cell viability. RESULTS: NSS demonstrated dose-dependent gastroprotection with superior efficacy compared to ranitidine. While ranitidine effectively reduced macroscopic damage and TNF-α mRNA expression, it showed no significant effects on IL-1β expression or JNK, p38, AKT, and NF-κB signaling pathways. In contrast, NSS significantly suppressed pro-inflammatory cytokines and comprehensively inhibited multiple molecular pathways including MAPK, AKT, and NF-κB activation across all doses. In vitro studies confirmed dose-dependent suppression of TNF-α-induced inflammatory gene expression (IL-6, IL-8, IL-1β, COX-2) without cytotoxicity. CONCLUSION: NSS exhibits gastroprotective effects through multi-target anti-inflammatory mechanisms. These mechanistic advantages over conventional acid-suppressive therapies suggest NSS as a promising candidate for preclinical and translational studies evaluating its clinical applicability in inflammatory gastric conditions.

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