Aim To study effects of berberine on the proliferation a nd differentiation of HL-60 cells. Methods Cell inhibitory effec t was determined by growthcurve method and colony formation.Cell differentiation was analyzed by cytomorphological changes, NBT reduction and cell surface antig en.Cell cycle was analyzed by flow cytometry.Results The growth o f HL-60 cells was significantly inhibited by berberine in a time and dose-depe ndent manner.1,2,4,8 mg?L -1 berberine induced differentiation of HL-60 c ells: Morphological evaluation indicated that the berberine-treated cells exhibited granulation appearance; NBT reduction was significantly increase d; expression of CD11b increased obviously. Flow cytometry analysis showed that berberine arrested HL-60 cells in G 0/G 1 phase, the percent of the cells in S phase decreased.Conclusion Berberine can induce differentiatio n and growth inhibition of HL-60 cells

AIM: To investigate the effects of lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) on the expression of MCP-1 in the cultured human unbilical vein endothelial cells (HUVECs). METHODS: Cultured HUVECs was incubated with ox-LDL, or preincubated with carrageenan and polyinosinic acid. LOX-1 and MCP-1 mRNA and protein were determined by RT-PCR and Western blot. RESULTS: Incubation of HUVECs with ox-LDL (from 0-100 mg/L) for 24 h markedly increased the expression of LOX-1 and MCP-1 (mRNA and protien) in a concentration-dependent fashion. Preincubation of HUVECs with carrageenan and polyinosinic acid, the chemical inhibitors of LOX-1, for 2 h, ox-LDL-mediated upregulation of LOX-1 and MCP-1 was suppressed (P

Shape-memory polymers(SMPs) can retain a temporary shape after pre-deformation at an elevated temperature and subsequent cooling to a lower temperature.When reheated,the original shape can be recovered.The development of the research on polyolefin,polyurethanes,polyester and some other shape-memory polymers were introduced and their applications in medical equipment were reviewed.

The adhesion of leukocytes to vascular endothelium is crucial for the generation of inflammatory responses. The selectins and ?2-integrin (Mac-1) play a major role in the process. Recently, it was reported that RO-heparin can inhibit selectin-mediated leukocyte adhesion. The effect of RO-heparin on the Mac-1-mediated neutrophils adhesion were further tested. The results showed that RO-heparin could effectively inhibit neutrophils binding to ICAM-1, adhering to COS-7 cells expressing human ICAM-1, and adhering to human umbilical vein endothelial cells (HUVECs) under static and flow conditions. The findings suggest that the effect of RO-heparin on leukocyte adhesion is mainly due to its inhibition on the interaction between selectins or Mac-1 and their ligands and that RO-heparin might be useful in preventing inflammation diseases.

Objective To investigate the prevention and cure effects of irbesartan on diabetic nephropathy.Methods The tissues of kidneys were harvested for histomorphometry and transmission electron microscope observation.The nuclear factor-?B(NF-?B) activity was measured by electrophoretic mobility shift assays(EMSA) in renal tissue and the level of TNF-? was measured by radio-immunity in serum.Results The glomerular basement membrane thickening,the numbers of total glomerular cells and monocyt cells in a glomerulus in experimental group were less than those of the control group.The NF-?B activity and TNF-? level were positively correlated with glomerular basement membrane thickening.Conclusion The irbesartan can prevent and cure diabetic nephropathy by inhibiting NF-?B and depressing inflammatory response.

The adhesion of leukocytes to vascular endothelium is crucial for the generation of inflammatory responses. The selectinsand β2-integrin (Mac-1) play a major role in the process. Recently, it was reported that RO-heparin can inhibit selectin-mediated leukocyte adhesion. The effect of RO-heparin on the Mac-1-mediated neutrophils adhesion were further tested. The results showed that RO-heparin could effectively inhibit neutrophils binding to ICAM-1, adhering to COS-7 cells expressing human ICAM-1, and adheringto human umbilical vein endothelial cells (HUVECs) under static and flow conditions. The findings suggest that the effect of RO-heparin on leukocyte adhesion is mainly due to its inhibition on the interaction between selectins or Mac-1 and their ligands and that RO-heparin might be useful in preventing inflammation diseases.

BACKGROUND: The oxidation of low density lipoprotein (LDL) is a key influencing factor in the occurrence and development process of atherosclerosis. How is the merit of the method for the detection of the level of anti-serum oxidized LDL (ox-LDL) antibody on the evaluation of atherosclerotic plaque?OBJECTIVE: To study the method for the detection of serum anti-ox-LDL antibody in mice with apolipoprotein E (Apo-E) genetic defect to analyze the merits of serous level of anti-ox-LDL antibody on the evaluation of the area of atherosclerotic plaque in mice with Apo-E genetic defect.DESIGN: Single factor analysis of variance (a case-controlled study)SETTING: Laboratory of nutrition and metabolism diseases in a university.PARTICIPANTS: Mice with Apo-E genetic defect were grouped into positive group (series: C57B L/6J, n = 15), while normal mice were grouped into control group (series: C57BL/6J, n = 15).INTERVENTIONS: Mice of two groups were fed in separate cage on laminar flow shelf for free drinking and eating. The venous blood was drawn from the orbit of mice after 16 weeks for the separation of mice serum. The level of anti-ox-LDL antibody was detected by enzyme-linked immunosorbent assay (ELISA) in the separated serum from either mice with Apo-E genetic defect or normal mice. The area of atherosclerotic plaque was measured by image analysis after oil red O staining.MAIN OUTCOME MEASURES: ox-LDL level and atherosclerotic plaque area in mice with Apo-E genetic defect or normal mice.RESULTS: Anti-ox-LDL antibody level of mice with Apo-E genetic defect was[ (0. 079 ±0. 028)% ], which was significantly higher than [(0. 012± 0.001 )% ] of normal mice ( F= 10. 666, P ＜ 0.01 ). The area of atherosclerotic plaque of mice with Apo-E genetic defect was (26. 25 ± 9.20) %, which was also significantly higher than 0% of normal mice, and moreover, there was a significant correlation between these two factors ( r =0. 638, P ＜ 0.01).CONCLUSION: Serum level of anti-ox-LDL antibody in mice with Apo-E genetic defect is closely correlated with the area of atherosclerotic plaque,which is an important indicator for the generation of atherosclerosis in mice with Apo-E genetic defect.

In recent years,many new microtubule-associated proteins are found or studied extensively in the treatment of breast cancer.End-binding protein 1 (EB1)has the promotional effects on cell proliferation and enhances the carcinogenesis of breast cancer,and also can affect the chemosensitivity of the treatment. MAP7 domain-containing protein 3 (Mdp3)expresses in breast epithelial cells and plays an important role on the growth and metastasis.Nucleolar and spindle-associated protein (NuSAP)gene is up-regulated in breast cancer and is considered as a biomarker for breast cancer.Tau expression level has a strong correlation with estrogen receptor (ER),progesterone receptor (PR)and human epidermal growth factor receptor-2 (HER-2), and it remains controversial in the results of the effect of paclitaxel chemotherapy and hormone treatment.

Aim To investigate the effect of probucol on reverse cholesterol transport from macrophage to feces in vivo,serum lipid profiles of mice were tested before and after probucol administration for 4 weeks,and the 3H-contents in serum,liver and feces in mice were quantitated after 24 hours intraperitoneally injected macrophages which were labeled with 3H cholesterol.Methods 32 C57BL/6 mice were treated with different probucol(0,0.1%,0.5%,1% W/W)in chow diet for 4 weeks,then these mice were injected intraperitoneally with RAW264.7 macrophages(0.5 ml?mice,cells 5.0?106 with 6.2?106 cpm)which were loaded with cholesterol by incubation with acetylated LDL,labeled with 3H-cholesterol.Serum profiles were quantitated by enzymatic method;serum and liver tissues were harvested at 24th hour,feces were collected(0~24 hs),and all were analyzed for tracer counts(all were expressed as the percentage of the total injected counts per minute).Results After 4 weeks 0.1% probucol administration,the levels of total cholesterol(TC),high-density lipoprotein cholesterol(HDL-C)decreased markedly by 34.3%,52.8%,(P