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https://www.selleckchem.com/products/donafenib-sorafenib-d3.html EVO reduced the susceptibility to DSS-induced destruction of epithelial integrity and severe inflammatory response, and regulated the gut microbiota and metabolites. Fecal Microbiota Transplantation (FMT) alleviated DSS-induced colitis, increased the abundance of L. acidophilus and the level of acetate. Furthermore, gavaged with L. acidophilus reduced pro-inflammatory cytokines, promoted the increase of goblet cells and the secretion of antimicrobial peptides, regulated the ratio of Firmicutes/Bacteroidetes and increased the level of acetate. Our results indicated that EVO mitigation of DSS-induced colitis is associated with increased in L. acidophilus and protective acetate production, which may be a promising strategy for treating UC.The vascular endothelium is one of the first barriers encountered by drugs and xenobiotics, which, once administered, enter the blood stream and diffuse to all organs through blood vessels. The continuous exposure of endothelial cells to drugs and chemical compounds turns out to be a huge risk for the cardiovascular system, as these substances could compromise endothelial vitality and function and create irreparable, localized or systemic damages. For this reason, a special attention should be paid to the safety of developing drugs on the cardiovascular system. In this study we focused our attention on carbonic anhydrase (CA)-IX inhibitors. CA-IX is an enzyme over-expressed in tumor cells in response to hypoxia, which is involved in pH control of the neoplastic mass microenvironment and in tumor progression. Specifically, we evaluated the safety on human umbilical vein endothelial cells (HUVEC) of CA-IX inhibitor AA-06-05, compared to its lead compound SLC-0111, for which the efficacy on tumor cells has already been proven. In this analysis we detected an impairment in viability and mitochondrial metabolism of HUVECs treated with AA-06-05 (but not with SLC-0111) in the c

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