G protein-coupleed receptor kinases (GRKs)not only regulates phosphorylation of G protein-coupled receptor which mediates receptor desensitization and initiates profound impairment of receptor signaling,but also regulates G protein and cytoskeleton. Meanwhile GRKs are regulated by protein kinase A, protein kinase C,actin and calcium/calmodulin. Surface of cell has many kinds of G protein-coupled receptor such as PAF receptor, histamine receptor, thrombine receptor which initiates signal effect of cell injury induced by inflammatory mediator. So GRKs have a certain regulatory role in the process of inflammation-induced cell injury through phosphorates G protein-coupled receptor.

Aim To investigate the mechanism of platelet-activating factor(PAF) induced injury on the cultured rat pulmonary microvascular endothelial cells(RPMVEC),and the interfering action of breviscapine. Methods RPMVEC were isolated from Wistar rat and cultured in vitro, the effects of PAF on morphology,monolayer permeability and F-actin of RPMVEC were observed, F-actin expression was evaluated by flow cytometry. Results PAF in the concentration over 0.1 mg?L -1 induced detachment and rupture of RPMVEC within 48 h. 10 mg?L -1 of PAF increased permeability of RPMVEC monolayer and induced depolymerization of F-actin within 120 min.Breviscapine inhibited these effects of PAF. Conclusion ①The detachment and rupture of RPMVEC induced by PAF depends on the exposed concentration and time.②The increased permeability of RPMVEC monolayer induced by PAF is significantly correlated with the depolymerization of F-actin. ③The increased permeability of RPMVEC monolayer and depolymerization of F-actin induced by PAF can be markedly inhibited by breviscapine, which exerts protective action on RPMVEC injury induced by PAF.

Objective · To observe the vascular structure before autogenous arteriovenous fistula (AVF) construction in patients with end-stage renal disease (ESRD) and analyze the risk factors of the pre-existing venous neointimal hyperplasia. Methods · The 8 vein samples were screened from 20 ESRD patients at their first time of the AVF construction (non-stenosis group), and the other 8 vein samples were screened from 15 ESRD patients at their at least second time of the AVF repair operation (stenosis group). Sections were prepared and stained with hematoxylin & eosin (H-E) or Masson's trichrome for observation. The intimal thickness was measured by the cellSens software, and its correlation with patients' renal function, calcium-phosphorus metabolism, iron metabolism and inflammatory reaction in the non-stenosis group were analyzed. Results · In the non-stenosis group, there were varying degrees of intimal hyperplasia in 5 (62.5%) cases, loss of endothelial cell layer in 3 (37.5%) cases, and vascular wall replacement by collagenous with atrophy or loss of muscle layer in 5 (62.5%) cases. In the stenosis group, almost all vein samples showed general thickening of the wall and 2 (25.0%) totally lost the muscle layer. Avg It of those two groups were statistically significant (P<0.01). In the non-stenosis group, both of average I/M thickness and average I/M area were negatively related to glomerular filtration rate (GFR) (P<0.05) and positively related to serum phosphorus and calcium-phosphorus product (P<0.05). Conclusion · Some apparently normal vein of ESRD patients showed varying degrees of intimal hyperplasia before AVF construction. The intimal hyperplasia had a remarkable correlation with GFR or calcium-phosphorus metabolism. Early intervention of the intimal hyperplasia prior to AVF construction may be a new prevention and control means.

AIM: To determine if aquaporin-1 (AQP-1) expression and function is influenced after lipopolysaccharide (LPS) stimulation in rat lung microvessel endothelial cells and to investigate the mechanisms of lung fluid abnormal metabolism in acute lung injury. METHODS: LPS at different concentrations (100 ?g/L, 1 mg/L or 10 mg/L) was used to stimulate cultivated rat lung microvessel endothelial cells in vitro at different stimulatory times (4 h, 12 h or 24 h), respectively. Tritium water permeation was conducted for determining the intracellular signal intensity in rat lung microvessel endothelial cells. The RT-PCR technique was applied for the assay of the expression of AQP-1 mRNA. RESULTS: The signal intensity of intracellular tritium water in the LPS stimulation group was less than that in normal control significantly. Compared with the normal control group (P