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https://www.selleckchem.com/products/Lapatinib-Ditosylate.html Dexamethasone is a common synthetic glucocorticoid drug that can promote foetal lung maturity. An increasing number of studies have shown that prenatal dexamethasone exposure (PDE) can cause a variety of short-term and long-term hazards to offspring, including bone development toxicity. H-type vessels are a newly discovered subtype of blood vessels associated with promoted bone formation and maintenance of bone mass. In this study, we aimed to explore whether H-type blood vessels are involved in PDE-induced long bone development toxicity in offspring and its mechanism. In vivo, we injected dexamethasone (0.2 mg/kg.d) subcutaneously at gestational days 9-20 and observed the H-type vessel abundance and bone mass at different time points in the offspring rats. In vitro, we investigated the effect of dexamethasone (0, 20, 100, and 500 nM) on the tube formation function of rat bone marrow-derived endothelial progenitor cells (EPCs) and explored its mechanism. Our results showed that the adult PDE female offspring ly intervention and therapeutic targets of foetal-derived osteoporosis.Ulcerative colitis (UC) is a chronic inflammatory bowel disease related to intestinal dysbiosis. Luteolin has been reported to reduce inflammation. However, it remains unclear whether luteolin ameliorates UC and regulates gut microbiota. In this study, we investigated the effects of luteolin on colonic structure and inflammation of dextran sulfate sodium (DSS)-induced rats using hematoxylin-eosin staining, immunohistochemistry and enzyme-linked immunosorbent assay and evaluated the effects of luteolin on gut microbiota using 16S rDNA sequencing. We found that luteolin treatment significantly reduced colonic damage, and inhibited colonic inflammation in UC rats, evidenced by the decreased levels of NF-κB, IL-17 and IL-23 in UC rats and the increased level of PPAR-γ. In addition, the 16S rDNA sequencing analysis revealed that luteol

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