Impact of nicotine on the interplay between human periodontal ligament cells and CD4+ T cells.

Periodontitis is a common infectious disease associated with destruction of periodontal ligaments and alveolar bones. CD4(+) T cell-mediated immune response is involved in the progression of periodontitis. Tobacco consumption increases the risk of periodontal disease. However, the impact of nicotine on the interaction between human periodontal ligament (PDL) cells and CD4(+) T cells remains unrevealed. Our study aims to investigate the effect of nicotine on PDL cells and the cocultured CD4(+) T cells. The PDL cell cultures were established by explants from healthy individuals, exposed to nicotine or α-bungarotoxin (α-BTX), and incubated solely or in combination with CD4(+) T cells. Afterwards, cell viability, secreted cytokines, and matrix metalloproteinases (MMPs) were evaluated. In monoculture of PDL cells, nicotine dramatically repressed cell viability and increased apoptosis. Meanwhile, α-BTX largely reversed the nicotine-induced apoptosis and increased viability of PDL cells. Compared with the monoculture, MMP-1, MMP-3, interleukin (IL)-1ß, IL-6, IL-17, and IL-21 in supernatant of cocultures were markedly elevated after treatment with nicotine. Moreover, α-BTX significantly attenuated nicotine-triggered production of these components either in mono- or co-cultures. In addition, PDL cell-derived CXCL12 following nicotine treatment recruited CD4(+) T cells. Above all, nicotine deteriorated periodontitis partially by promoting PDL cell-CD4(+) T cell-mediated inflammatory response and matrix degradation.

Ameloblasts serum-free conditioned medium: bone morphogenic protein 4-induced odontogenic differentiation of mouse induced pluripotent stem cells.

Induced pluripotent stem (iPS) cells possess the ability of self-renewal and can differentiate into cells of the three germ layers, both in vitro and in vivo. Here we report a new method to efficiently induce differentiation of mouse iPS cells into the odontogenic lineage. Using ameloblasts serum-free conditioned medium (ASF-CM), we successfully generated ameloblast-like cells from mouse iPS cells. Importantly, culturing mouse iPS cells in ASF-CM supplemented with BMP4 (ASF-BMP4) promoted odontogenic differentiation, which was evident by the upregulation of ameloblast-specific as well as odontoblast-specific genes. On the other hand, culturing mouse iPS cells in ASF-CM supplemented with noggin (ASF-noggin), an inhibitor of BMP4, abrogated this effect. These results suggest that mouse iPS cells can be induced by ASF-BMP4 to differentiate into ameloblast-like and odontoblast-like cells. The results of our study raise the possibility of using patient-specific iPS cells for tooth regeneration in the future. Copyright © 2016 John Wiley & Sons, Ltd.

Correlation between high density lipoprotein and monocyte subpopulations among stable coronary atherosclerotic heart disease patients.

High density lipoprotein (HDL) is a structurally and functionally heterogeneous molecular particle whose function is unclear in atherosclerosis at present. Studies show that small HDL functional imbalance may exist in Coronary Atherosclerotic Heart Disease (CAD) patients. Monocyte is considered to play an important role in atherosclerosis, in accordance with the expression of superficial CD14 and CD16, it can be divided into three subpopulations. The purpose of this study was to explore the relation between HDL and monocyte subpopulations among CAD patients. We report 90 cases of stable CAD patients and define the monocyte subpopulations as classical monocyte (CD14++CD16-; CM), intermediate monocyte (CD14+CD16+; IM), and non-classical monocyte (CD14+CD16++; NCM); HDL group is measured by polyacrylamide gel electrophoresis. The results indicated that the small HDL in blood serum has a correlation with proinflammatory NCM in circulation but a negative correction with CM and no relationship with diabetes, saccharify hemoglobin, hypertension, smoking history and taking dose of statins drugs and severity of disease. In conclusion, this study primarily confirms that micromolecule HDL level correlates with the increase of non-classical monocyte subpopulations and decrease of classical monocyte quantity. Thus demonstrates the proinflammatory correlation between micromolecule HDL and internal immunity in the development of stable atherosclerosis.

Blood lipid profiles and factors associated with dyslipidemia assessed by a point-of-care testing device in an outpatient setting: A large-scale cross-sectional study in Southern China.

OBJECTIVE: To promote the concept of POCT and to investigate dyslipidemia in Guangzhou, China, we performed a study examining blood lipids assessed by POCT and reported factors associated with dyslipidemia. DESIGN AND METHODS: This multicenter, cross-sectional study enrolled outpatients from 9 Guangzhou hospitals from May through September 2013. After informed consent was obtained, the following information was collected: age; gender; the presence of diabetes mellitus, obesity, and hypertension as well as current use of cigarettes or alcohol. Patients were asked to fast for 8h before the blood examination performed on a POCT device, the CardioChek PA. RESULTS: Of 4012 patients enrolled (1544 males, 2468 females; mean age 60.35±9.41 years), 1993 (49.7%) patients had dyslipidemia, but only 101 (5.1%) took statins. The multivariate tests of associations between demographic variables, comorbidities, and the risk of having dyslipidemia found that the significant predictors of dyslipidemia were male gender, age ≥60 years, being a current smoker or alcohol drinker, and hypertension. CONCLUSION: Most dyslipidemia patients in Guangzhou remain untreated. POCT in China is feasible, and its widespread use might improve dyslipidemia awareness, treatment and control.

Long-term efficacy of transcatheter closure of ventricular septal defect in combination with percutaneous coronary intervention in patients with ventricular septal defect complicating acute myocardial infarction: a multicentre study.

AIMS: To assess the immediate and long-term outcomes of transcatheter closure of ventricular septal defect (VSD) in combination with percutaneous coronary intervention (PCI) in patients with VSD complicating acute myocardial infarction (AMI). METHODS AND RESULTS: Data were prospectively collected from 35 AMI patients who underwent attempted transcatheter VSD closure and PCI therapy in five high-volume heart centres. All the patients who survived the procedures were followed up by chest x-ray, electrocardiogram and echocardiography. Thirteen patients underwent urgent VSD closure in the acute phase (within two weeks from VSD) while the others underwent elective closure at a median of 23 days from VSD occurrence. The percentage of VSD closure device success was 92.3% (36/39) and procedure success was 91.4% (32/35). The incidence of in-hospital mortality was 14.3% (5/35). At a median of 53 months follow-up, only two patients died at 38 and 41 months, respectively, and other patients' cardiac function tested by echocardiography improved significantly compared to that evaluated before discharge. CONCLUSION: The combination of transcatheter VSD closure and PCI for treating VSD complicating AMI is safe and feasible and is a promising alternative to surgery in patients with anatomically suitable VSD and coronary lesion.

Nicotine favors osteoclastogenesis in human periodontal ligament cells co-cultured with CD4(+) T cells by upregulating IL-1ß.

Periodontitis, which is the main cause of tooth loss, is one of the most common chronic oral diseases in adults. Tooth loss is mainly a result of alveolar bone resorption, which reflects an increased osteoclast formation and activation. Osteoclast formation in periodontal tissue is a multistep process driven by osteoclastogenesis supporting cells such as human periodontal ligament (PDL) cells and CD4(+) T cells. Inflammatory cytokines, such as interleukin-1ß (IL-1ß), can induce osteoclastogenesis by affecting the expression of receptor activator of NF-κB ligand (RANKL) and osteoprotegerin (OPG) in human PDL cells. Nicotine, the major component in tobacco smoking and a specific agonist of the α7 nicotinic acetylcholine receptor (α7 nAChR), has been proven to regulate the expression of inflammatory cytokines in smoking-associated periodontitis. In this study, we investigated the mechanism(s) through which nicotine affects osteoclastogenesis in human PDL cells co-cultured/non-co-cultured with CD4(+) T cells. Human PDL cells were stimulated with nicotine (10-5 M) and/or α-bungarotoxin (α-BTX, specific antagonist of α7 nAChR, 10-8 M) before being co-cultured with CD4(+) T cells. Compared with mono-culture systems, stimulation with nicotine caused an increased secretion of IL-1ß in serum of human PDL cell-CD4(+) T cell co-culture, and the expression of RANKL in human PDL cells was further upregulated co-cultured with CD4(+) T cells, while no differences were observed in the expression of OPG between the co-culture and mono-culture systems. Our data suggested that nicotine upregulated IL-1ß secretion, further upregulated RANKL expression in smoking-associated periodontitis, which may aid in the better understanding of the relationship between nicotine and alveolar bone resorption.

AP-1 and NF-κB transcriptionally regulate interleukin-8 in EA.Hy926 cells under shear stress.

Cardiovascular and cerebrovascular diseases remain the leading cause of death in the world. AS (atherosclerosis) is not only an inflammatory disease in which chemokines play the main role but also a disorder that is related to blood SS (shear stress). We have investigated the action of IL-8 (interleukin-8) mRNA expression in human endothelial cells line-EA.Hy926 under SS at different intensities and duration. Expression increases with time in an intensity dependent manner. With regard to the transcriptional mechanism involved, transient transfection of the human wild-type IL-8 promoter (-162/+44)/luciferase reporter plasmid, or site mutation of one of the binding sites [AP-1 (activator protein 1) or NF-κB (nuclear factor κB)] in the IL-8 promoter region was investigated. Both AP-1 and NF-κB were essential for SS-activated transcription, with the cells responding to NF-κB activation within minutes. After stimulated at low SS (4.20 dyne/cm2) for 30 min, the P65 subunit was translocated from the cytoplasm to nucleus for at least 60 min, while the cytoplasmic level of IκB (inhibitory κB) gradually decreased. The combined activation of NF-κB and AP-1 are the upstream regulators of low SS-induced IL-8 production in EA.Hy926 cells, which subsequently trigger an inflammatory reaction in endothelium.

Targeting nicotinic acetylcholine receptor to treat smoking-related periodontitis.

Tobacco smoking is considered to be one of the major risk factors for periodontitis. Nicotine, the major component in tobacco smoke, has been considered playing an important role in tobacco-related morbidity by acting through the nicotinic acetylcholine receptors (nAChRs) expressed by non-neuronal cells. Recently studies found that nAChRs could be expressed on oral gingival and periodontal tissues. We hypothesize that nicotine may act on periodontal tissues directly and specifically through nAChRs to affect periodontitis activity, and that nicotine-induced periodontitis could be prevented by tissue-selective nAChR inhibitors targeting periodontal nAChRs. Thus, periodontal nAChRs may provide to be novel molecular targets to treat smoking-related periodontitis, effectively blocking of periodontal nAChRs may offer an optimistic outlook for the therapy of smoking- related periodontitis.

Functional expression of alpha 7 nicotinic acetylcholine receptors in human periodontal ligament fibroblasts and rat periodontal tissues.

Tobacco smoking is the main risk factor associated with chronic periodontitis, but the mechanisms that underlie this relationship are largely unknown. Recent reports proposed that nicotine plays an important role in tobacco-related morbidity by acting through the nicotinic acetylcholine receptors (nAChRs) expressed by non-neuronal cells. The aim of this study was to investigate whether alpha 7 nAChR was expressed in periodontal tissues and whether it functions by regulating IL-1 beta in the process of periodontitis. In vitro, human periodontal ligament (PDL) cells were cultured with 10(-12) M of nicotine and/or 10(-9) M of alpha-bungarotoxin (alpha-Btx), a alpha 7 nAChR antagonist. The expression of alpha 7 nAChR and IL-1 beta in PDL cells and the effects of nicotine/alpha-Btx administration on their expression were explored. In vivo, an experimental periodontitis rat model was established, and the effects of nicotine/alpha-Btx administration on expression of alpha 7 nAChR and development of periodontitis were evaluated. We found that alpha 7 nAChR was present in human PDL cells and rat periodontal tissues. The expressions of alpha 7 nAChR and IL-1 beta were significantly increased by nicotine administration, whereas alpha-Btx treatment partially suppressed these effects. This study was the first to demonstrate the functional expression of alpha 7 nAChR in human PDL cells and rat periodontal tissues. Our results may be pertinent to a better understanding of the relationships among smoking, nicotine, and periodontitis.

[Effects of high-density lipoprotein on the cholesterol efflux from endothelial cells].

OBJECTIVE: To study the effects of high-density lipoprotein (HDL) and oxidized high-density lipoprotein (ox-HDL) on the expression of ATP-binding cassette transporter A1 (ABCAl) and cholesterol efflux in human umbilical vein endothelial cells (HUVECs). METHODS: In vitro cultured HUVECs were incubated in the presence of 100 microg/ml HDL or 100 microg/ml ox-HDL for 24 h, using PBS as the negative control. ABCA1 mRNA level and cholesterol efflux rate were determined using RT-PCR and a liquid scintillator, respectively. RESULTS: HDL and ox-HDL significantly elevated the level of ABCA1 mRNA by 58% and 23% relative to the control level, respectively (P<0.05). The cholesterol efflux rate in ox-HDL group was significantly lower than that in HDL group (P<0.01). CONCLUSION: HDL increases ABCAl expression and cholesterol efflux in HUVECs. Oxidative modification of HDL decrease cholesterol efflux by inhibiting the expression of ABCAl, suggesting a possible mechanism of ox-HDL in the pathogenesis of atherosclerosis.

[Effect of Astragalus polysaccharides on the phenotype and functions of human dendritic cells in vitro].

OBJECTIVE: To assess the effect of astragalus polysaccharides (APS) in inducing phenotypic and functional changes of human dendritic cells (DCs) in vitro. METHODS: Human dendritic cells were induced from the peripheral blood monocytes in vitro by the application of tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4) and GM-CSF, and cultured in the presence of APS at different concentrations (50, 100, and 200 mg/L). The morphological changes of the DCs were identified by optical microscope or scanning electron microscope. The phenotypic alterations of the cells were analyzed by flow cytometry. RESULTS: The DCs cultured for 24 h in the presence of LPS and APS at 50 and 100 mg/L showed suspended growth in the culture medium and underwent morphological changes from spherical cells to irregular cells, with rough cell surface and cell processes of different morphologies. APS-treated DCs had the most typical dendritic structures and highly expressed the phenotypic markers of DCs (CD86 and HLA-DR), but with down-regulated CD14 expression as shown by flow cytometry. CONCLUSION: Both APS and the cytokines can induce the maturation of DCs derived from peripheral blood monocytes.

[Classification and functional study of peripheral blood dendritic cells in patients with coronary artery disease with different atherosclerotic plaques].

OBJECTIVE: To study the quantitative and functional changes of peripheral blood dendritic cells (DCs) and their subsets in the leukocyte population in patients with coronary artery disease (CHD) with different coronary artery plaques and explore the relation between DCs and coronary plaque development. METHODS: Thirty CHD patients were divided into SAP (10 cases), UAP (10 cases) and ACS (10 cases) groups, with another 10 patients having negative result in coronary angiography as the control group. Intravascular ultrasound (IVUS) was performed to identify the nature of the plaques. The percentage and absolute number of peripheral blood DCs and DC subsets were measured by flow cytometry. The functional status of the DCs was analyzed by enzyme-linked immunosorbent assay (ELISA) and flow cytometry. RESULTS: In the SAP group, IVUS found stable plaques in 8 cases and unstable plaques in 2 cases; in UAP group, 7 patients had unstable plaques, 2 had stable plaques, and 1 had plaque rupture. Plaque rupture, unstable plaques and stable plaques were found in 6, 3 and 1 patients in ACS group, respectively. In comparison with patients with stable plaques, those with unstable plaques had significantly increased percentages and number of DCs, mDCs and mDC1 (P<0.05), while the mDC2s and pDCs showed no obvious difference between them (P>0.05). The percentages and number of DCs, mDCs, mDC1s and pDCs were significantly decreased in patients with ruptured plaques (P<0.05). In peripheral blood monouclear cells cultured for 7 days, the CD83 expression was significantly higher in unstable and rupture plaque groups than in stable plaque group, and no significant difference was found between stable plaque group and the control group (P>0.05). In unstable and rupture plaque groups, co-culture with 2x10(5)/ml DCs evoked strong proliferation of the T cells in comparison with the stable plaque group, but no difference was found between the stable plaque and the control groups (P>0.05). Significantly higher levels of interleukin-2 and interferon-alpha were detected in the supernatant of the mixed lymphocyte reaction in unstable and ruptured plaque groups than in stable plaque and control groups, without obvious difference between the latter two groups. CONCLUSION: The percentage and absolute number of peripheral blood DCs and their functional status suggest the alterations of the coronary artery plaques in CHD patients.

[Effects of high-density lipoprotein 1 on the formation of foam cells from human monocyte-derived macrophages].

OBJECTIVE: To investigate effects of serum HDL(1) on the formation of foam cells from human peripheral blood monocyte-derived macrophages. METHODS: Sectie density polyacrylamide gel electrophoresis (sd-PAGE) was applied for isolation and preparation of HDL(1) simultaneously. Monocytes were isolated from human peripheral blood by Ficoll-Hypaque density gradient centrifugation and plastic adsorptive process. The isolated monocytes were stimulated by phorbol 12-myristate 13-acetate (PMA) at a concentration of 50 nmol/L for 48 h and transferred to macrophages. The monocyte-derived macrophages were then coincubated with 80 mg/L ox-LDL and HDL(1) (0, 0.1, 1.0 and 10.0 mg/L) for 6, 12 and 24 h, respectively. The formation of foam cells was identified by transmission electron microscope (TEM), total cholesterol (TC), free cholesterol (FC) and protein (Pro) in cultured cells were quantitatively analyzed by high performance chromatography (HPLC) and modified lowry protein assay, respectively. RESULTS: HDL(1) isolated from human serum by sd-PAGE could significantly decrease TC/Pro ratio in foam cells in a concentration-dependent (0 mg/L: 36.9 +/- 1.1, 10.0 mg/L: 6.2 +/- 0.4, P < 0.01) and time-dependent (10.0 mg/L HDL(1) 6 h: 16.9 +/- 0.9, 24 h: 6.4 +/- 0.6, P < 0.01) manner. CONCLUSION: HDL(1) is capable of inhibiting and attenuating the formation of foam cells by decreasing cellular TC, therefore, might play an important role in attenuating atherosclerosis.

[Evaluation of a rabbit model of abdominal aorta atherosclerosis].

OBJECTIVE: To explore the methods for non-invasive evaluation of a rabbit model of aorta atherosclerosis model. METHODS: Sixteen male New Zealand rabbits (n=16) were randomized into the experimental group and control group and fed with high-cholesterol diet and normal diet after balloon injury in the abdominal aorta, respectively. Eight weeks later, pathological examination, angiography and surface ultrasonography were carried out to evaluate the plaques in the aorta. RESULTS: After feeding with high-cholesterol diet for 8 weeks, the weight, total cholesterol (TC), triglycerides (TG) and low-density lipoprotein (LDL) were significantly increased in the rabbits (P<0.001), and atherosclerosis in the abdominal aorta was directly observed using angiography and surface ultrasonography. The rate of vasoconstriction showed significant difference between the experimental group and control group (t=5.921, P=0.000). In the experimental rabbits, the vasoconstriction increased obviously after drug stimulation with high lumen eccentricity index. A significant positive correlation was noted between the lumen eccentricity index and the rate of vasoconstriction (r=0.983, P=0.000). CONCLUSION: A rabbit model of abdominal aorta atherosclerosis can be established rapidly by balloon injury and high-cholesterol diet. The aortic wall thickness, lumen diameter and lumen eccentricity index determined by surface ultrasonography can be used to evaluate the validity of the model establishment and the nature of the plaque.

[Oxidized low-density lipoprotein enhances the expressions of SREBP-2 and HMGCR mRNA in macrophages derived from the monocytes of patients with acute coronary syndrome].

OBJECTIVE: To investigate the effect of oxidized low-density lipoprotein (ox-LDL) on the expressions of sterol regulatory element binding protein-2 (SREBP-2) and hydroxymethylglutaryl CoA reductase (HMGCR) in the macrophages derived from monocytes of patients with acute coronary syndrome (ACS). METHODS: LDL was oxidized by Cu2+ to prepare ox-LDL, and peripheral monocytes were isolated by density gradient centrifugation from patients with ACS diagnosed by coronary arteriography. Macrophages derived from the monocytes after phorbol myristate acetate (PMA) stimulation were treated with ox-LDL at the concentrations of 0, 20, 40, and 100 ng/ml, and the changes in the expressions of SREBP-2 and HMGCR were detected by real-time RT-PCR. RESULTS: Compared with the control cells, the macrophages treated with ox-LDL showed significantly increased expressions of SREBP-2 and HMGCR mRNA (P<0.05). In cells treated with ox-LDL, the expressions of SREBP-2 and HMGCR mRNA differed significantly with the dose administered (P<0.05). CONCLUSION: Within a defined dose range, ox-LDL can dose-dependently enhance the expressions of SREBP-2 and HMGCR mRNA in macrophages from patients with ACS.

Effects of nicotine on alveolar bone loss in experimental periodontitis in rat: a micro-computed tomographic analysis / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To establish the three-dimensional images of rat's alveolar bone and to evaluate the effects of nicotine on alveolar bone loss during the process of ligature-induced periodontitis with micro-computed tomography (micro-CT).</p><p><b>METHODS</b>Thirty-six adult male SD rats received silk ligatures around the cervix of the right second maxillary molars. Then the animals were randomly assigned to three groups and received daily intraperitoneal injections as follows: group A (control), saline solution; group B, nicotine, 0.83 mg x kg(-1) x d(-1); and group C, nicotine, 1.67 mg x kg(-1) x d(-1). Six animals in each group were randomly selected and sacrificed at day 14 and 28. Micro-CT examinations were used to evaluate the periodontal breakdown.</p><p><b>RESULTS</b>With the nicotine dose increased, bone mineral density (BMD), bone volume fraction (BVF), and trabecular thickness (TT) gradually reduced, while the trabecular spacing (TS) and alveolar bone loss (ABL) increased. At day 28, the ABL of group C (left, right) was (0.61 +/- 0.14) mm and (1.39 +/- 0.09) mm, and significantly higher than that of group B [(0.39 +/- 0.10) mm and (1.31 +/- 0.06) mm] and group A[(0.30 +/- 0.06) mm and (0.94 +/- 0.07) mm]. The BMD of group C, group B and group A at day 28 was [(617.86 +/- 34.27), (572.46 +/- 31.62) mg/cm3], [(660.04 +/- 36.73), (604.97 +/- 32.59) mg/cm3] and [(709.15 +/- 34.95), (657.04 +/- 30.06) mg/cm3] respectively.</p><p><b>CONCLUSIONS</b>Daily administration of nicotine results in significant bone loss and microstructure deteriorations in the trabeculae of alveolar bone.</p>

[Peripheral dendritic cell subpopulation changes in patients with coronary artery disease].

OBJECTIVE: To compare the peripheral dendritic cell subpopulation changes in patients with or without coronary artery disease. METHODS: A total of 60 patients with angiographic documented coronary artery disease (CAD) were recruited in this study, including 20 cases with acute myocardial infarction (AMI group), 20 cases with unstable angina(UA group) and 20 patients with stable angina (SA group). Eleven patients with chest pain and without coronary stenosis served as chest pain control (CPS group). Ten cases without heart diseases served as normal control (Normal control group). Numbers of peripheral myeloid dendritic cell (mDC) and plasmacytoid dendritic cell (pDC) precursors were determined by FACS. RESULT: The proportions of mDC precursors were significantly lower in UA group and AMI group (4.7% +/- 2.6%, 5.0% +/- 2.7%) than that in SA, CPS and control groups (11.0% +/- 6.4%, 12.0% +/- 3.9%, 12.3% +/- 3.3%, respectively, all P < 0.001). pDC numbers were similar among groups. CONCLUSION: Reduced circulating mDC subsets in patients with unstable angina and AMI might suggest enhanced mDC recruitment to vulnerable plaques in these patients.

[Effect of rosiglitazone on tumor necrosis factor-alpha-induced nuclear factor-kappaB and coupling factor 6 expressions in human umbilical vein endothelial cells].

OBJECTIVE: To investigate the effect of rosiglitazone on the expression of nuclear factor-kappaB (NF-kappaB) and coupling factor 6 (CF6) induced by tumor necrosis factor-alpha (TNF-alpha) in cultured human umbilical vein endothelial cells (HUVEC). METHODS: Cultured HUVEC of passage 3-5 were stimulated with TNF-alpha and then cultured in the presence of rosiglitazone. The expression of CF6 and NF-kappaB subunit p65 were evaluated by immunocytochemistical method. RESULTS: Pretreatment of HUVECs with rosiglitazone inhibited TNF-alpha-induced expression of CF6 in a dose-dependent manner. The activation of CF6 stimulated by TNF-alpha was suppressed by ROS in a dose-dependent manner. CONCLUSION: TNF-alpha-induced enhancement of the gene expression and release of CF6 is mediated by activation of NF-kappaB signaling pathway. ROS can inhibit the activation of IKK, block NF-kappaB signaling pathway and inhibit the expression of CF6, which may be the mechanism underlying the action of TZDs on hypertension.

[Association of dendritic cell distribution with intima hyperplasia in rats with diabetes mellitus].

OBJECTIVE: To investigate the association of dendritic cell distribution in the peripheral blood, spleen and arterial wall with intimal hyperplasia in rats with diabetes mellitus. METHODS: Diabetes mellitus was induced in rats by intraperitoneal injection of streptozotocin and high-fat feeding for 8 weeks. Peripheral blood, arterial wall and the spleen were collected from the rats to prepare cell suspensions, in which the proportions of dendritic cells and T cells were determined by flow cytometry. RESULTS: The tunica intimal hyperplasia was more obvious in diabetic rats with or without high-fat feeding as compared with that of the control rats (P<0.05), and their dendritic cells decreased significantly in the peripheral blood (P<0.05) but increased in the arterial wall. The percentage of T cells was also increased in the peripheral blood and arterial wall of the diabetic rats. CONCLUSION: Changes in the distribution of dendritic cells and T cells are closely associated with intimal hyperplasia in diabetic rats, suggesting the involvement of dendritic cells and T cells in the formation of atherosclerosis.