ABSTRACT
BACKGROUND:Generaly, the stent surface modification, especialy seeding cels, may accelerate or cause stent endothelium, and cause restenosis for prevention of in-stent thrombosis. OBJECTIVE: To develop the optimal conditions for vascular stents coated with bone marrow mesenchymal stem cels. METHODS: Cerebrovascular stent was co-cultured with passage 3 bone marrow mesenchymal stem cels from rats at 1×106, 1×107, 1×108, and 1×109/L. Cels on the stents were examined with transmission electron microscopy after 48 hours. A total of 160 male Sprague-Dawley rats were enroled, among which, 20 rats were as normal control group, and the remaining 140 were used for producing models of ischemic stroke that were randomly sub-divided into seven groups at 8 weeks after modeling: stainless steel stent implanted group, polymer stent group, and different concentrations of cellstent composite groups. After 8 weeks of implantation, the expression of vascular endothelial growth factor in these cels was examined by western blot assay. Rat platelet activation in different groups was determined by flow cytometry. RESULTS AND CONCLUSION:Implanted stem cels were able to grow adherently on the stainless steel stent wal. When the planting cellconcentration was 1×107 cels/L, the cels and organeles were morphologicaly normal and covered the stent surface wel. These coated cels also expressed vascular endothelial growth factor, suggesting that they functioned as endothelial cels, and they also significantly lowered platelet activation. When co-cultured with 1×107/L bone marrow mesenchymal stem cels, the stent was covered wel with endothelial-like cels and had significant lower platelet activationin vivo.
ABSTRACT
There was no significant increase of serum glucocorticoid in partial adrenalectomized rats after scalding, whereas glucocorticoid receptor in hepatic cytosol of those rats tended to increase. And 6 h after scalding, the difference between scalded and controlled rats was highly significant. Hepatic glucocorticoid receptor mRNA was also determined by the method of dot blot. It was found that hepatic gluco corticoid receptor mRNA of partial adrenalectomized rats was increased 6h after scalding. Those results suggest that the decrease of hepatic cytosol glucocorticoid receptor in scalded intact rats was dependent on the rise of serum glucocorticoid.
ABSTRACT
Phospholipase A2(PLA2) activity in rat serum and honiogenate of liver and lungs was determined by the method of titrating.It was found that serum PLAi activity of adrenalectornized rats(ADX) was 75.13 + 7.94 U, which was significantly different from that of control rats (58.88 ?15.33U).When ADX were injected with hydrocortisone(5 mg/100g tody weight) and decapitated 2h later, the serum FLA2 activity was 55.09?8.63U, which did not differ significantly from that of controls.However, the PLAi activity in the homogenate of lungs and.liver had no significant change.These results show that glucocorticoids exerted tonic inhibition of rat serum PLA2.
ABSTRACT
Previous work in our laboratory showed that, after scalding, there was not only a decrease of rat liver cytosol [3H]-Dexamethasone specific binding sites but also an increase of apparent dissociation constant of [3H]-Dex and a change of sedimentation coefficient of glucocorticoid receptor (GCR).The present study was carried out using photoaffinity labeling of GCR in rat liver cytosol.It was found that there was no significant difference between molecular weights of . GCR in normal and scalded rats determined by SDS-polyacrylamide gel electrophoresis. Our result suggests that change of sedimentation coefficient is not due to alteration of molecular weight of GCR binding subunit.