Inflammatory bowel disease is known as the most chronic inflammatory disorder in colon, which subsequently progresses to intestinal obstruction and fistula formation. Many studies to date for the treatment of IBD have been focused on inflammation. However, most of the anti-inflammatory agents do not have anti-fibrotic effects and could not relieve intestinal stricture in IBD patients. Because preventing or reversing intestinal fibrosis in IBD is a major therapeutic target, we analyzed the papers focusing on TGF-β signaling in intestinal fibrosis. TGF-β is a good candidate to treat the intestinal fibrosis in IBD which involves TGF-β signaling pathway, EMT, EndMT, ECM, and other regulators. Understanding the mechanism involved in TGF-β signaling will contribute to the treatment and diagnosis of intestinal fibrosis occurring in IBD as well as the understanding of the molecular mechanisms underlying the pathogenesis.

Quinazolines are a class of nitrogen-containing heterocyclic compounds with broad-spectrum of pharmacological activities. Transition-metal-catalyzed reactions have emerged as reliable and indispensable tools for the synthesis of pharmaceuticals. These reactions provide new entries into pharmaceutical ingredients of continuously increasing complexity, and catalysis with these metals has streamlined the synthesis of several marketed drugs. The last few decades have witnessed a tremendous outburst of transition-metal-catalyzed reactions for the construction of quinazoline scaffolds. In this review, the progress achieved in the synthesis of quinazolines under transition metal-catalyzed conditions are summarized and reports from 2010 to date are covered. This is presented along with the mechanistic insights of each representative methodology. The advantages, limitations, and future perspectives of synthesis of quinazolines through such reactions are also discussed.

Xanthohumol prevents dextran sulfate sodium-induced colitis via inhibition of IKK/NF-B signaling in mice Xanthohumol prevents dextran sulfate sodium-induced colitis via inhibition of IKKβ/NF-κB signaling in mice