OBJECTIVE: Increasing of adhesion between leukemia cells and endothelial cells during all-trans retinoic acid (ATRA) treatment plays an important role in retinoic acid syndrome. This work observed the effects of tripterine on this ATRA-caused increasing in adhesion. METHODS: The effects of tripterine on ATRA-induced expressions of adhesive molecules in acute promyelocytic leukemia cell line NB4 and human umbilical vascular endothelial cells (HUVEC) were detected by flow cytometry. The effects of tripterine on adhesion between ATRA-treated NB4 and HUVEC were determined by adhesive assays. RESULTS: ATRA caused remarkable elevation of intercellular adhesion molecule-1 (ICAM-1) in NB4 cells, which could be significantly reduced by tripterine (P<0.01). The expressions of E-selectin, vascular cell adhesion molecule-1 (VCAM-1) and ICAM-1 in HUVEC were elevated by conditioned medium from ATRA-induced NB4 (ATRA-NB4-CM) (P<0.01), and inhibited by tripterine with inhibition rates being 25.3%, 42.4% and 61.0% respectively. ATRA increased the adhesion between NB4 and HUVEC, which was reversed completely by tripterine. CONCLUSION: Tripterine can inhibit ATRA-caused adhesion between leukemia cells and endothelial cells, and it might be a potential agent for treating retinoic acid syndrome.

ObjectiveTo explore the release of exogenous growth factors from small intestinal submucosa (SIS) in bladder regeneration. MethodsThe release of vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) from SIS in vitro were evaluated by ELISA and MTT method. The defected bladder walls of rats in experimental group were repaired with porcine small intestinal submuscosa. Partial bladder mucosa and smooth muscle of the rats in control groups were destroyed. At regular intervals, the VEGF and bFGF expression were observed by histological and immunohistochemical methods. ResultsThe concentration of bFGF and VEGF released in vitro from SIS in PBS solution were (121.8±2.683) ng/L and (93.8±3.033) ng/L respectively, and showed proliferation of vascular endothelial cell. In the SIS framework, the capillary and smooth muscle were observed followed histological evaluation. The weak expression of VEGF and bFGF in both experimental and control groups were found in the first week. Since the second week the VEGF and bFGF expression in experimental group began to increase with a peak in the 6th week, and began to decrease after 8 weeks. In the control group, the weak VEGF and bFGF expression were shown during the observation. ConclusionSIS functions as a carrier for exogenous growth factors release in rat bladder regeneration.