Inflammatory bowel disease (IBD) is characterized by chronic and relapsing intestinal inflammation, which currently lacks safe and effective medicine. Some previous studies indicated that Astragaloside IV (AS-IV), a natural saponin extracted from the traditional Chinese medicine herb Ligusticum chuanxiong, alleviates the experimental colitis symptoms in vitro and in vivo. However, the mechanism of AS-IV on IBD remains unclear. Accumulating evidence suggests that M2-polarized intestinal macrophages play a pivotal role in IBD progression. Here, we found that AS-IV attenuated clinical activity of DSS-induced colitis that mimics human IBD and resulted in the phenotypic transition of macrophages from immature pro-inflammatory macrophages to mature pro-resolving macrophages. In vitro, the phenotype changes of macrophages were observed by qRT-PCR after bone marrow-derived macrophages (BMDMs) were induced to M1/M2 and incubated with AS-IV, respectively. In addition, AS-IV was effective in inhibiting pro-inflammatory macrophages and promoting the pro-resolving macrophages to ameliorate experimental colitis via the regulation of the STAT signaling pathway. Hence, we propose that AS-IV can ameliorate experimental colitis partially by modulating macrophage phenotype by remodeling the STAT signaling, which seems to have an essential function in the ability of AS-IV to alleviate the pathological progress of IBD.

Metabolic reprogramming is a hallmark of cancer, which is still far from being fully understood in colorectal cancer. In order to characterize the metabolic changes in colorectal cancer, we performed...

AIM: Abdominal aortic aneurysm (AAA) is characterized by macrophage polarization, and at present, no drug therapy is available. Although grape-seed polyphenols (GSP) showed an anti-AAA effect, the role of GSP in the phenotype shift in macrophages remains unknown. METHOD: The main phenolic compounds in GSP were determined by LC-MS. Male C57BL/6 mice were divided into four equal groups, namely sham group, CaPO 4 group, CaPO 4 +GSP low-dose group, and CaPO 4 +GSP high-dose group. GSP was administered intragastrically after CaPO 4 application. Molecular expressions were histologically evaluated and analyzed by various staining assays and FACS. RESULTS: GSP administration inhibited CaPO 4-induced AAA formation, which correlated with a decrease in macrophage infi ltration and retainment of vascular smooth muscle layer as compared to those in the CaPO 4 group. FACS assay showed that the GSP administration dose-dependently decreased the CD54 expression (low-dose group: 11.4 ± 2.1 % and high-dose group: 4.8 ± 1.4 % vs 23.2 ± 3.6 %; p < 0.05 and p < 0.01, respectively) and increased the CD206 expression of F4/80-positive cells in GSP-administered groups as compared with that in CaPO 4-injured aortas in the CaPO 4 group (low-dose group: 22.4 ± 3.3 % and highdose group: 26.7 ± 4.2 % vs 8.1 ± 1.3 %; p < 0.05 and p < 0.01, respectively).