Peptic ulcer disease (PUD) is a multifactorial and complex disease caused by an imbalance of protective and aggressive factors (endogenous and exogenous). Despite advances in recent years, it is still responsible for substantial mortality and triggering clinical problems. Over the last decades, the understanding of PUD has changed a lot with the discovery of Helicobacter pylori infection. However, this disease continues to be a challenge due to side-effects, incidence of relapse from use of various anti-ulcer medicines, and the rapid appearance of antimicrobial resistance with current H. pylori therapies. Consequently, there is the need to identify more effective and safe anti-ulcer agents. The search for new therapies with natural products is a viable alternative and has been encouraged. The literature reports the importance of monoterpenes based on the extensive pharmacological action of this class, including wound healing and anti-ulcerogenic agents. In the present study, 20 monoterpenes with anti-ulcerogenic properties were evaluated by assessing recent in vitro and in vivo studies. Here, we review the anti-ulcer effects of monoterpenes against ulcerogenic factors such as ethanol, nonsteroidal anti-inflammatory drugs (NSAIDs), and Helicobacter pylori, highlighting challenges in the field.Biomolecules 2020, 10, 265 2 of 18 PUD results from an imbalance in mucosal defensive factors, such as mucus secretion, bicarbonate efflux, endogenous antioxidant, cell regeneration, continuous synthesis and release of prostaglandin E 2 (PGE 2 ), nitric oxide (NO), and sulfhydryl compounds (SH); and aggressive agents such as smoking, alcohol consumption, dietary factors, stress, prolonged and excessive intake of nonsteroidal anti-inflammatory drugs (NSAIDs), and Helicobacter pylori (H. pylori) infection, among others [6][7][8][9]. For a long time, it was believed that the main factor implicated in the development and progression of peptic ulceration was an hypersecretory acidic environment and together with dietary factors and/or stress was thought to cause most of PUD. But the discovery of H. pylori infection and the widespread use of NSAIDs in the second half of the 20 th century changed this perception. In recent years, peptic ulcer has been found to have multiple causes-H. pylori infection, NSAIDs, smoking, alcohol consumption, stress, lifestyle, and genetic predispositions are determined as major risk factors for the development of PUD [2].
PathophysiologyUnder normal conditions, gastric and duodenal mucosa integrity is maintained by the mucus-bicarbonate barrier, the neutral pH, and continuous epithelial cell renewal [10,11]. PGE 2 stimulates cell proliferation, mucus, and bicarbonate production, promoting a crucial function in mucosa preservation. Another vital factor in gastric homeostasis is adequate blood flow. The NO and PGs are responsible for the maintenance of proper perfusion to the gastric mucosa, assuring the delivery of oxygen and nutrients, as well as removing toxic metabolites, preventing damages to the ti...
