Gastric ulcer is a chronic disease featured with unexpected complications, including bleeding, stenosis and perforation, as well as a high incidence of recurrence. Clinical treatments for gastric ulcer have allowed the rapid development of potent anti-ulcer drugs during the last several decades. Gastric ulcer healing is successful with conventional treatments including H2-receptor antagonists, and proton pump inhibitors (PPIs) have been essential for ulcer healing and prevention of complications. Additionally, Helicobacter pylori eradication therapy is effective in reducing ulcer recurrence and leads to physiological changes in the gastric mucosa which affect the ulcer healing process. However, in spite of these advancements, some patients have suffered from recurrence or intractability in spite of continuous anti-ulcer therapy. A new concept of the quality of ulcer healing (QOUH) was initiated that considers the reconstruction of the mucosal structure and its function for preventing ulcer recurrence. Although several gastroprotection provided these achievements of the QOUH, which PPI or other acid suppressants did not accomplish, we found that gastroprotection that originated from natural products, such as a newer formulation from either Artemisia or S-allyl cysteine from garlic, were very effective in the QOUH, as well as improving clinical symptoms with fewer side effects. In this review, we will introduce the importance of the QOUH in ulcer healing and the achievements from natural products.

Background: Downregulation of TGF‐β receptors is implicated in colon cancer development. Inactivation of either of the two transmembrane serine/threonine kinases, TGF‐β1 types I/II receptors, is now implicated in carcinogenesis, especially gastrointestinal carcinogenesis.Methods: We generated transgenic mice, called pS2–dnRII or ITF–dnRII, of which the dominant negative mutant of the TGF‐β type II receptor was expressed under the control of tissue‐specific promoters, the pS2 promoter for stomach and ITF for intestine. They were either infected with H.pylori (ATCC 43504 strain, CagA⁺ and VacA⁺) or administered with azoxymethane to determine the significance of loss of TGF‐β signalling in gastrointestinal carcinogenesis.Results: Gastric adenocarcinoma developed in pS2–dnRII mice, whereas only chronic active gastritis was noted in wild‐type littermates after 36 weeks of H.pylori infection. Mice lacking in TGF‐β signalling specifically in the stomach showed a significantly higher proliferation cell nuclear antigen‐labelling index when infected with H.pylori than wild‐type littermates (P < 0.01). Development of colonic aberrant crypt foci was provoked in mice by intraperitoneal injections of azoxymethane, and ITF–dnRII mice showed significantly higher incidences of ACF and colon cancers than wild‐type littermates.Conclusions: Maintaining normal TGF‐β signalling in the gastrointestinal tract seems to be important either for preventing abnormal mucosal proliferation, or for suppressing or retarding carcinogenesis.