The results obtained in the present study showed that Chinese SC 560 herbal medicine QYHJ could significant suppress the production of CAF-derived CXCL1, 2 and 8, thereby preventing pancreatic cancer cell invasion. Thus, in this study, we have demonstrated that CAFs exhibited an enhanced capacity for inducing pancreatic cancer cell migration and invasion compared with NFs, while QYHJ-treated CAFs exhibited decreased migration and invasion-promoting capacities in vitro. In addition, we showed that QYHJ significantly suppressed CAF proliferation activities and the production of CAF-derived CXCL1, 2 and 8. Taken together, these results suggested that suppressing the tumor-promoting capacity of CAFs through Chinese herbal medicine attenuates pancreatic cancer cell invasion. Intestinal bowel disease is a chronically recurring inflammatory disorder arising from genetic predispositions and/ or environmental or immunological modifying factors that negatively affect the interaction between the commensal microflora and the intestinal mucosa. The two most common forms of IBD are Crohn��s disease and ulcerative colitis. These diseases often result in S 25585 morbidity due to a high incidence of diarrhea, abdominal pain, rectal bleeding and malnutrition. Despite significant progresses, our understanding of the inflammatory regulators that contribute to the pathogenesis of IBD is still limited. Recently, SIRT2, an NAD + -dependent sirtuin deacetylase, was revealed to play an important role in inflammation. SIRT2 belongs to a highly conserved family of NAD + -dependent enzymes, consisting of seven members, which vary in subcellular localizations and have substrates ranging from histones to transcription factors and enzymes. SIRT2 is primarily a cytosolic protein, but can shuttle into the nucleus, thus explaining its ability to deacetylate both cytosolic and nuclear substrates. In the present study, we identified a novel role for SIRT2 as a potential suppressor of DSS-induced colitis in the mouse. First by interfering with intestinal barrier function, then stimulating local inflammation and dysplasia, DSS-induced colitis resembles the clinical progression of human UC, representing an important model for the translation of mouse data to human disease relevance. Here we showed that SIRT2 deficiency led to a more severe colitis compared to that seen in Sirt2+/+ control mice. Although Sirt22/2 mice were indistinguishable from Sirt2+/+ mice, with respect to body weight and intestinal morphology, upon a DSS challenge they developed more severe colitis.