Gastroprotective triterpenoids: Pharmacological mechanism

Gastric and duodenal ulcers affect a considerable amount of people in the world. Ulcer occurs when there is a disturbance of the normal equilibrium caused by either enhanced aggression or diminished mucosal resistance of gastrointestinal tract. Mucosa defends gastrointestinal tract of acid, pepsin, bile, leukocyte infiltration and external substances such as alcohol, caffeine, chilli or certain drugs such as NSAIDs. The defense mechanisms of the gastrointestinal mucosa mainly consist of functional, humoral and neuronal factors. Mucus alkaline secretion, mucosal microcirculation and motility act as functional factors, while prostaglandins and nitric oxide (NO) act as humoral factors, and capsaicin-sensitive sensory neurons (CPSN) act as neuronal factors. Several plants containing triterpenoids have been shown to possess anti-ulcer activity. The gastroprotective effects of triterpenoids have been studied on ethanol or NSAIDs-induced gastric injury models. These models induced impairment in the mucosal defense process with the consequent gastric damage. The principal mechanism of gastroprotection of triterpenoids has been reported by the activations of mucous membrane secretion instead of the inhibition of gastric acid secretion. Chemically, this gastroprotective effect has been referred to the presence of a hydroxyl group free or derivative at position C-3 for sterols and triterpenoids. Some pharmacological gastroprotective mechanisms for this kind of natural products has been attributed to the role of prostaglandins, nitric oxide (NO), sulfhydryl groups (-SH), and capsaicin-sensitive afferent neurons. Besides, recently leukocyte adherence, TNF-α and hydrogen sulfide has been implicated on mucosal defense mechanism, however it is unknown on triterpenoids gastroprotection.