New and Emerging Treatment Strategies for Gastrointestinal Diseases, 2nd Edition

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: closed (25 June 2026) | Viewed by 1121

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Instituto de Pesquisa Pelé Pequeno Príncipe, Faculdades Pequeno Príncipe, Curitiba 80250-060, PR, Brazil
Interests: pharmacology; inflammatory bowel diseases; polysaccharides
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Special Issue Information

Dear Colleagues,

Gastrointestinal homeostasis is orchestrated by complex regulatory mechanisms, including a protective epithelial barrier, a diverse microbiota and a highly regulated immune response controlled by different mucosal cell types. However, disruption of these mechanisms can lead to the development of acute and/or chronic pathological processes characterized by widely recognized problems, including gastroesophageal reflux, peptic ulcers, bile acid disorder, inflammatory bowel disease and others. Current treatment options for problems related to the gastrointestinal tract are limited and do not fully meet the needs of patients. In addition, prolonged use of some medications can have serious adverse effects. Therefore, the search for new treatment options is necessary.

Original papers and review articles are welcome for the Special Issue, entitled ‘New and Emerging Treatment Strategies for Gastrointestinal Diseases, 2nd Edition’. Manuscripts must cover all aspects of the following:

  • Advances and challenges in the development of new and novel treatment strategies for gastrointestinal diseases.
  • Extraction/isolation and identification of extracts or bioactive compounds for the treatment of gastrointestinal diseases.
  • Benefits and safety of new treatment strategies for gastrointestinal diseases.

Dr. Daniele Maria-Ferreira
Guest Editor

Manuscript Submission Information

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Keywords

  • gastrointestinal diseases
  • gastrointestinal homeostasis
  • gastrointestinal injuries
  • gastrointestinal disturbances
  • dysbiosis
  • bile acid
  • inflammatory bowel diseases
  • diarrhea

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Published Papers (2 papers)

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Research

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23 pages, 34498 KB  
Article
Mechanism of Lian-Huo-Hua-Zhuo Formula in Alleviating Gastric Mucosal Inflammation in a Mouse Model of Chronic Atrophic Gastritis by Inhibiting the IL-17 Signaling Pathway
by Xiaoxuan Mo, Fan Gao, Jiaye Tian, Fengyue Xu, Zeyang Xie, Hongyan Wei, Jinhu Yang, Jianming Jiang, Guoxing Deng and Qiuhong Guo
Pharmaceuticals 2026, 19(7), 1043; https://doi.org/10.3390/ph19071043 (registering DOI) - 5 Jul 2026
Abstract
Background: Chronic atrophic gastritis (CAG) is a prevalent precancerous gastric disorder characterized by persistent inflammation, glandular atrophy, and progressive mucosal damage, for which effective multi-target therapeutic strategies remain insufficient. The Lian-Huo-Hua-Zhuo formula (LHHZ), a traditional Chinese herbal prescription, has demonstrated potential anti-inflammatory [...] Read more.
Background: Chronic atrophic gastritis (CAG) is a prevalent precancerous gastric disorder characterized by persistent inflammation, glandular atrophy, and progressive mucosal damage, for which effective multi-target therapeutic strategies remain insufficient. The Lian-Huo-Hua-Zhuo formula (LHHZ), a traditional Chinese herbal prescription, has demonstrated potential anti-inflammatory and gastrointestinal protective effects in clinical practice; however, its active constituents and mechanisms of action against CAG remain undefined. This study aimed to clarify the absorbed bioactive components of LHHZ and explore its therapeutic mechanism for CAG. Methods: Ultra-high-performance liquid chromatography coupled with quadrupole Orbitrap high-resolution mass spectrometry was employed to identify the absorbed components of LHHZ in the gastric and intestinal tissues of mice. The therapeutic effects of LHHZ on CAG were assessed through histopathological staining, ultrastructural observation, and evaluation of serum and gastric functional indicators. Network pharmacology, molecular docking, and molecular dynamics simulations were integrated to predict the core targets and key signaling pathways, while the regulatory effects on the interleukin-17 (IL-17) signaling pathway were further validated by immunofluorescence staining, real-time quantitative polymerase chain reaction, and Western blotting. Additionally, 16S ribosomal RNA gene sequencing and targeted metabolomics were applied to investigate the effects of LHHZ on gut microbiota composition and short-chain fatty acid (SCFA) metabolism. Results: The results revealed that 55 and 48 absorbed components were identified in the gastric and intestinal tissues, respectively, predominantly derived from Coptis chinensis Franch. and Pogostemon cablin (Blanco) Benth. LHHZ significantly alleviated gastric mucosal lesions, reduced intestinal metaplasia, restored the ultrastructure of gastric mucosal cells, improved gastric functional indicators including pepsinogen I (PG I), pepsinogen II (PG II), and gastrin-17 (GAS-17), and decreased the levels of pro-inflammatory cytokines. Network pharmacology combined with in vitro and in vivo experiments demonstrated that the core bioactive components of LHHZ can target and regulate interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α), attenuate activation of the IL-17 signaling pathway, and suppress the secretion of downstream pro-inflammatory factors. Furthermore, LHHZ enhanced the alpha diversity of gut microbiota, reduced the Firmicutes to Bacteroidetes (F/B) ratio, restored the abundance of SCFA-producing bacteria such as Bacteroidales and Oscillospirales, and normalized the aberrant levels of eight SCFAs. Significant correlations were also observed between gut microbiota composition and SCFA metabolism. Conclusions: These findings suggest that LHHZ alleviates CAG by inhibiting inflammation via the IL-17 signaling pathway and by modulating the gut microbiota–SCFA axis, thereby providing preclinical evidence supporting its further investigation and development for multi-target therapeutic strategies against CAG. Full article
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14 pages, 1068 KB  
Systematic Review
Efficacy and Safety of Tegoprazan in Helicobacter pylori Eradication: An Umbrella Review of Meta-Analyses
by Dmitrii N. Andreev, Alsu R. Khurmatullina, Igor V. Maev, Dmitry S. Bordin, Andrey V. Zaborovskiy, Yury A. Kucheryavyy, Filipp S. Sokolov and Petr A. Beliy
Pharmaceuticals 2026, 19(4), 637; https://doi.org/10.3390/ph19040637 - 17 Apr 2026
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Abstract
Objective: This umbrella review synthesizes and critically appraises the evidence on the efficacy and safety of tegoprazan-based versus proton pump inhibitor (PPI)-based regimens for Helicobacter pylori (H. pylori) eradication. Methods: This umbrella review was pre-registered in PROSPERO (CRD420251271120). Systematic reviews and [...] Read more.
Objective: This umbrella review synthesizes and critically appraises the evidence on the efficacy and safety of tegoprazan-based versus proton pump inhibitor (PPI)-based regimens for Helicobacter pylori (H. pylori) eradication. Methods: This umbrella review was pre-registered in PROSPERO (CRD420251271120). Systematic reviews and meta-analyses published between 1 January 2018 and 10 December 2025 were identified through MEDLINE/PubMed, EMBASE, and the Cochrane Library. Reviews comparing tegoprazan-based and PPI-based eradication regimens in adult patients were included. Methodological quality was assessed using AMSTAR-2, risk of bias with ROBIS, and certainty of evidence with GRADE. Pooled relative risks (RRs) were calculated, with subgroup analyses by study design, treatment duration, and therapeutic regimen. Results: Eight systematic reviews and meta-analyses encompassing 17 primary studies and 12,714 participants were included. Tegoprazan-based regimens were associated with a statistically significant improvement in eradication efficacy compared with PPI-based therapies (RR = 1.019; 95% CI: 1.003–1.035; p = 0.021). In randomized controlled trials, the benefit was more pronounced (RR = 1.037; 95% CI: 1.015–1.061; p = 0.001), whereas no statistically significant benefit was observed in non-randomized studies (RR = 1.014; 95% CI: 0.991–1.037; p = 0.235). The efficacy advantage was mainly confined to quadruple therapy regimens (RR = 1.044; 95% CI: 1.002–1.088; p = 0.038). Tegoprazan-based regimens were associated with a lower incidence of overall adverse events compared with the PPI group (RR = 0.930; 95% CI: 0.885–0.976; p = 0.003). Conclusions: Tegoprazan-containing regimens were associated with a modest but statistically significant improvement in H. pylori eradication compared with PPI-containing regimens, particularly in randomized controlled trials and quadruple therapy regimens. Full article
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