The Role of Triterpenoids in Gastric Ulcer: Mechanisms and Therapeutic Potentials

Abstract

Gastric ulcer (GU) is a prevalent gastrointestinal disorder impacting millions worldwide, with complex pathogenic mechanisms that may progress to severe illnesses. Conventional therapies relying on anti-secretory agents and antibiotics are constrained by drug abuse and increased bacterial resistance, highlighting the urgent need for safer therapeutic alternatives. Natural medicinal compounds, particularly triterpenoids derived from plants and herbs, have gained significant attention in recent years due to their favorable efficacy and reduced toxicity profiles. Emerging evidence indicates that triterpenoids exhibit potent anti-ulcer properties across various experimental models, modulating key pathways involved in inflammation, oxidative stress, apoptosis, and mucosal protection. Integrating current knowledge of these bioactive compounds facilitates the development of natural triterpenoids, addresses challenges in their clinical translation, deepens mechanistic understanding of GU pathogenesis, and drives innovation of therapeutic strategies for GU. This review comprehensively evaluates the progress of research on triterpenoids in GU treatment since 2000, discussing their biological sources, structural characteristics, pharmacological activities, and mechanisms of action, the animal models employed in the studies, current limitations, and the challenges associated with their clinical application.

Keywords: gastric ulcer; gastroprotective; pharmacological mechanism; triterpenoids.

Figure 1

Invasive factors and protective factors affecting the incidence of GU. Protective factors include mucus, bicarbonate, tight junction, prostaglandins, blood flow, and cell renewal. Invasive factors include smoking, NSAIDs, H. pylori, alcohol, pepsin, and gastric acid.

Figure 2

Protopanaxadiol type triterpenoids with anti-ulcer activity. (A) Ginsenoside Rb1; (B) Ginsenoside Rd; and (C) Ginsenoside Rg3.

Figure 3

Protopanaxatriol type triterpenoids with anti-ulcer activity. (A) Ginsenoside Rh4 and (B) protopanaxatriol.

Figure 4

The structure of ocotillol.

Figure 5

The structure of astragaloside IV.

Figure 6

The structure of 3α-hydroxymasticadienoic acid.

Figure 7

Oleanane-type triterpenoids with anti-ulcer activity. (A) Oleanolic acid; (B) Araloside A; (C) 18β-Glycyrrhetinic Acid; (D) Soyasaponin Bb; (E) δ-Amyrone; (F) Maslinic acid; and (G) α-Boswellic acid.

Figure 8

Ursane-type triterpenoids with anti-ulcer activity. (A) Ursolic acid; (B) Tormentic acid; (C) Asiaticoside; and (D) Niga-ichigoside F1.

Figure 9

Lupane-type triterpenoids with anti-ulcer activity. (A) Lupeol and (B) Betulinic acid.

Figure 10

The structure of friedelin.

Figure 11

The structure of azadiradione.

Figure 12

The pharmacological mechanisms of triterpenoids in the prevention and treatment of GU. Triterpenoids can prevent and treat GU through various pathways, such as the redox balance, inflammation, cytoprotective factor, gastric juice, apoptosis, regeneration, and antibacterial pathways.

Figure 13

The relationship between experimental animal models of GU and human GU. Previous studies utilized diverse GU models, including ethanol, NSAIDs, pylorus ligation, restraint water-immersion, and acetic acid-induced GU models. These models, respectively, correspond to alcohol consumption, long-term NSAID use, excessive gastric acid, stress-induced GUs, and chronic GU.