Fine particulate matter (PM2.5) not only directly damages lung tissue, but also can be absorbed into blood through alveolar capillaries, which is toxic to the cardiovascular system. PM2.5 can affect lipid metabolism, endothelial function, coagulation and thrombosis through oxidative stress, inflammatory reaction, autonomic nervous dysfunction and immune regulation abnormality, so that it promote arteriosclerosis, plaque instability, and increase the morbidity and mortality of cardiovascular disease. We reviewed the effects and mechanisms of PM2.5 on arteriosclerosis, in order to provide the evidence for the studies into prevention of cardiovascular diseases caused by air pollution.

Objective To investigate the different influences of simvastatin on proliferation of rat smooth muscle progenitor cells(SPCs) versus endothelial progenitor cells (EPCs) and identify the compounds that differentially inhibit SPCs and EPCs proliferation for clinical usefulness. Methods Total mononuclear cells (MNCs) were isolated from bone marrow of rats by Fieoll density gradient centrifugation, and then the cells were plated on fibronectin-coated culture dishes. SPCs outgrew from the culture of MNCs in the presence of platelet-derived growth factor-BB and basic fibroblast growth factor, whereas EPCs were obtained in the presence of vascular endothelial growth factor. SPCs were identified as adherent cells positive for α-smooth muscle actin (α-SMA) by indirect immunofluoreseent staining. EPCs were characterized as adherent cells double positive for DiLDL-uptake and lectin binding by direct fluorescent staining. SPCs and EPCs were stimulated by simvastatin (0.01～10.00 μmol/L) or vehicle control for the respective time points (6 h, 12 h, 24 h and 48 h). SPCs and EPCs proliferation were assayed with 3H-TdR incorporation and manual counting respectively. Results Simvastatin obviously inhibited SPCs proliferation. At the concentration of 0. 01 μmol/L for 12 h,simvastatin significantly reduced the number of SPCs by (5.8±3.1)% compared with control group (P<0.05). Simvastatin significantly stimulated EPCs proliferation, which was dose- and time dependent and reached maximum at 1 μmol/L after 24 hours (2.0±0.1 fold increase, P<0.01).Conclusions Simvastatin displays different effects on SPCs (inhibited) and EPCs (promoted)proliferation. Local application of simvastatin may inhibit arterial restenosis and promote reendothelialization of injured vessels.

Objective:To conduct a clinical tretrospective study on the effect of Silymarin Meglumine Tab on acute and chronic hepatitis B and to explore the related clinical significance. Methods: 41 cases and 205 cases of hospitalized patients pathologically diagnosed as acute and chronic hepatitis B respectively by liver tissuse puncture were divided into three group: ① Silymarin Meglumine Tab group; ② Ganyanling group; ③ complex group consisting of Silymarin Meglumine Tab and Gangyanling and diammonium glycyrrhizinate. To detect the index of routine liver function test before and after the treatment and analyze the hospitalization treatment course. Results: Compared with before treatment, liver functions of acute and chronic hapatitis B were improved to certain extent within each group after treatment (P0.05). The hospitalization treatment time of acute hepatitis B of the three group were almost the same, but the hospitalization treatmeng time of chronic hepatitis B of the Silymarin Meglumine Tab group was 2-4days less than that of the Ganyanling group and the complex group. Conclusion: As far as Silybini Meglumine Tab was concerned, it was better for chronic hepatitis B than acute hepatitis B because it was less complicated to administer the medicine, relieving the liver's burden of metabolism, and hospitalization treatment time was shorter, relieving patients' financial burden,which suggested that it was important to administer proper amount of medicine while taking into consideration protecting the liver's compensation function. If consideration was given to stimulating liver microcirculation with small dosage of TCM, so as to promote the exchange of the liver metabolite in blood, or detoxication and expulsion of toxin, it was likely to be more advantageous to the restoration of liver function and the liver tissue structure.

OBJECTIVETo observe the effect of platelet derived growth factor receptor β (PDGFR-β) transfected endothelial progenitor cells (EPCs) on vascular regeneration.

METHODSSpleen-derived mononuclear cells (MNCs) were isolated using density gradient centrifugation and induced with special culture medium. EPCs transfection was performed with Lipofectamine(TM) 2000 reagent according to the instruction manual. Carotid artery injury was induced in splenectomized mice. EPCs were injected by tail vein immediately and at 24 h after endothelial injury of the carotid artery. Evans blue staining was performed to evaluate reendothelialization at 7 days after endothelial injury of the carotid artery.

RESULTSMost adherent cells were LDL and UEA-I double positive. Laser scanning confocal microscopy showed that transfection efficiency was about 50%-60%. The reendothelialized area in the PDGFR-β-EPCs group was significantly larger than that in EGFP-EPCs group.

CONCLUSIONTransplantation of PDGFR-β over-expressed EPCs can promote reendothelialization in the early phase after carotid artery injury.

Animals ; Carotid Artery Injuries ; pathology ; surgery ; Cells, Cultured ; Disease Models, Animal ; Endothelial Cells ; cytology ; metabolism ; transplantation ; Endothelium, Vascular ; cytology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Platelet-Derived Growth Factor ; genetics ; metabolism ; Regeneration ; Stem Cell Transplantation ; Stem Cells ; cytology ; metabolism