The association between the microbes in the tracheobronchial aspirate fluid and bronchopulmonary dysplasia in preterm infants.

OBJECTIVE: The study aimed to evaluate the association between microbes in the lower respiratory tract (LRT) and the srisk for severe bronchopulmonary dysplasia (sBPD) in premature infants. METHODS: We conducted a retrospective, single-center study of preterm infants who were admitted to the neonatal intensive care unit (NICU) of Southern Medical University Affiliated Maternal & Child Health Hospital of Foshan, China, between January 2015 and December 2017. The microbes in the LRT were screened by using tracheobronchial aspirate fluid (TAF) culture. RESULTS: One hundred and fifty-five infants were included in the analysis. Among 155 infants, 41 were diagnosed with sBPD, and 114 were diagnosed without sBPD. There were significant differences between infants with and without sBPD in regard to birth weight (BW), gestational age (GA), the duration of endotracheal ventilation and supplemental oxygen. The incidence of retinopathy (ROP) and sepsis was higher in the sBPD infants than in the infants without sBPD. There was a difference in the detection rate of Gram-negative bacteria (GNB) between the two groups. Stenotrophomonas maltophilia and Klebsiella pneumoniae were mainly detected in TAF. CONCLUSIONS: The LRT microbes were different between infants with and without sBPD, and GNB is more frequently detected in sBPD infants.

Efficacy of intra-arterial catheter-directed thrombolysis for popliteal and infrapopliteal acute limb ischemia.

OBJECTIVE: The purpose of this study was to examine the efficacy and safety of catheter-directed thrombolysis (CDT) for first-line treatment of popliteal and infrapopliteal acute limb ischemia. METHODS: A total of 28 consecutive patients (30 limbs) who underwent CDT for treatment of popliteal and infrapopliteal acute limb ischemia of thromboembolic origin between March 2012 and December 2017 were enrolled in this study. Per the Society for Vascular Surgery, limbs were classified into three runoff score groups: <5, good; 5 to 10, compromised; and >10, poor. The primary end points were primary patency and limb salvage assessed by Kaplan-Meier survival analysis. Secondary end points were technical success and clinical success. The Society for Vascular Surgery-recommended scale for gauging changes in clinical status was used to assess clinical success. Safety of the procedure was evaluated on the basis of periprocedural complications according to the Society of Interventional Radiology classification system. RESULTS: Technical success was achieved in 25 (83.33%) treated limbs. Improved clinical status (grade +3/+2) was achieved in 93.33% of limbs. Primary patency and limb salvage for the entire cohort were 76.67% and 90% at 6 months and 60.0% and 76.67% at 12 months, respectively. The patency rate at 6 months and 12 months was 91.67% and 83.33% for the good runoff group, 80% and 60% for the compromised runoff group, and 50% and 25% for the poor runoff group, respectively. The patency rate of the good runoff group was significantly higher compared with that of the poor runoff group (P = .004). Major amputation rate and mortality rate were 16.67% and 7.14%, respectively, at 12 months. The reintervention rate was 3.57% at 6 months and 21.42% at 12 months. CONCLUSIONS: CDT is safe and effective for revascularization of smaller vessel acute arterial thromboembolism as a primary therapy. However, more studies with a larger sample are warranted.

Effects of Left Gastric Artery Ligation Versus Sleeve Gastrectomy on Obesity-Induced Adipose Tissue Macrophage Infiltration and Inflammation in Diet-Induced Obese Rats.

BACKGROUND Bariatric procedures such as left gastric artery ligation (LGAL) and sleeve gastrectomy (SG) have emerged as important procedures for treating morbid obesity. In this study, we compared the effects of LGAL vs. SG on obesity-induced adipose tissue macrophage infiltration and inflammation in diet-induced obese rats. MATERIAL AND METHODS Sprague-Dawley (SD) rats were fed a high-fat diet (HFD) for 16 weeks to induce obesity. SG, GLAL, or corresponding sham surgeries were performed in anesthetized rats. Inflammatory factor expression in serum and epididymal and retroperitoneal adipose tissues were analyzed 4 weeks after surgery. Macrophage infiltration and phenotype transformation were also assessed with Western blot analysis and immunofluorescence. RESULTS Both LGAL and SG strongly attenuated high-fat diet (HFD)-induced fat accumulation in retroperitoneal and epididymal tissues. The expressions of inflammatory cytokines such as tumor necrosis factor (TNF)-alpha, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1 were downregulated after LGAL and after SG by promoting activation of M2 macrophages, despite continued exposure to HFD. Furthermore, both LGAL and SG resulted in increased macrophage infiltration, but did not contribute to phenotype transformation of macrophages to M1. CONCLUSIONS LGAL and SG both reduced fat accumulation caused by HFD feeding. Therapies designed to ameliorate the inflammatory response by promoting activation of M2 macrophages may be valuable.

[Composition, Spatial Distribution Characteristics and Source Analysis of Chromophoric Dissolved Organic Matter in the Lanzhou Reach of the Yellow River].

Chromophoric dissolved organic matter (CDOM) in riverine systems can be affected by environmental conditions and land-use, and can thus provide important information regarding anthropogenic activities in surrounding landscapes. It can modify the optical properties of waters and affect the balance and availability of dissolved nutrients and metals in water bodies. However, the characteristics of CDOM in the Lanzhou reach of the Yellow River have not yet been reported. In this study, the optical properties of water samples collected at 32 locations during April 2017 across the Lanzhou reach of the Yellow River were examined using UV-VIS and excitation-emission matrix fluorescence spectroscopy-parallel factor analysis (EEM-PARAFAC), to determine CDOM compositional changes, spatial distribution characteristics, and sources. Cluster analysis was used to categorize samples into groups of similar pollution levels within a study area. Results showed that CDOM was primarily comprised of low molecular weight organic substances with aromatic structure belonging to complex "protein-like-humic-like" substances, and dominated by protein-like substances (organism sources). Two humic-like components (C1, C4), one tryptophan-like component (C2), and one non-humic-like component (C3) were identified by PARAFAC. Tryptophan-like substances were predominant in the components of CDOM, accounting for 51.06% of average total fluorescence intensity. Humic-like materials and non-humic-like substances accounted for 36.74% and 12.20%, respectively. Weak correlations were observed between protein-like substances and humic-like substances, indicating different sources of these components. The distribution of total fluorescence intensity showed a distinct spatial pattern; trends in fluorescence intensity were weak-strong-weak along an upstream to downstream continuum, mainly affected by changes in the content of protein-like substances. The spatial variation of the CDOM in the Lanzhou reach of the Yellow River can therefore be assessed based on protein-like materials dynamics. Public spaces along rivers offer opportunities for community gatherings and recreational activities. However, high-intensity anthropogenic activities strongly influence CDOM concentration and composition in this area in different ways; sources include increased residential/commercial wastewater, catering, water recreation facilities pollution, shipping, and a small amount of industrial discharge. In addition, it was concluded that endogenetic pollution may become the main source of internal loading in the Lanzhou reach of the Yellow River, implying that stronger endogenetic pollution control is needed to alleviate CDOM pollution and improve water quality.

[Adsorption Characteristics of Norfloxacin by Biochars Derived from Reed Straw and Municipal Sludge].

Two types of biochars were prepared by pyrolyzing reed straw and municipal sludge at the temperature of 500 degrees C. The structure and properties of biochars were characterized by BET, scanning electron microscope (SEM), energy dispersive spectroscopy (EDS) and fourier transform infrared spectroscopy ( FTIR ). The effects of pH value, adsorption time, temperature and initial concentration of norfloxacin (NOR) on the adsorption behaviors were determined by single factor experiments, which were used to preliminarily discuss adsorption mechanism. The results showed that the adsorption of NOR onto biochars derived from reed straw and municipal sludge could reach 70% and 60% of the total adsorption within 12 h, respectively; the maximum adsorption capacities of the two biochars were 2.13 mg x g(-1) (biochar derived from reed straw) and 2.09 mg x g(-1) (biochar derived from municipal sludge). The quantities of both absorptions increased with the decreasing solution pH. The two adsorption kinetics of NOR onto biochars followed the pseudo second order kinetic equations, and adsorption isotherms fitted well with the Langmuir equations. Adsorption thermodynamics parameters such as Gibbs free energy (AG), enthalpy (AH) and entropy (AS) indicated that the two adsorptions were endothermic reactions. Infrared spectroscopy analysis indicated that oxygen-containing functional groups on biochars provided NOR molecules with adsorptive sites, which facilitated the formation of hydrogen bonds between NOR and the biochars.

Linking Colleague Support to Employees' Promotive Voice: A Moderated Mediation Model.

Promotive voice is essential for improving team and organization performance. Yet in the current literature, less was known regarding the psychological reasons why people engage in promotive voice. Through the lens of social exchange, we proposed that employees who received support from colleagues may develop higher level of felt obligation for constructive change which leads to promotive voice. Analyses of multi-source data from 51 cross-functional sources (51 team supervisors and 162 employees) showed that employees' felt obligation for constructive change positively mediates the relationship between colleague support and promotive voice behavior. Moreover, the impact of colleague support on felt obligation for constructive change is stronger when there is a low level of subgroup formation in the team. Theoretical and practical implications of these findings are discussed.

Curcumin attenuates lipolysis stimulated by tumor necrosis factor-α or isoproterenol in 3T3-L1 adipocytes.

BACKGROUND AND AIM: Curcumin, an active component derived from dietary spice turmeric (Curcuma longa), has been demonstrated antihyperglycemic, antiinflammatory and hypocholesterolemic activities in obesity and diabetes. These effects are associated with decreased level of circulating free fatty acids (FFA), however the mechanism has not yet been elucidated. The flux of FFA and glycerol from adipose tissue to the blood stream primarily depends on the lipolysis of triacylglycerols in the adipocytes. Adipocyte lipolysis is physiologically stimulated by catecholamine hormones. Tumor necrosis factor-α (TNFα) stimulates chronic lipolysis in obesity and type 2 diabetes. In this study, we examined the role of curcumin in inhibiting lipolytic action upon various stimulations in 3T3-L1 adipocytes. METHODS: Glycerol release from TNFα or isoproterenol-stimulated 3T3-L1 adipocytes in the absence or presence of curcumin was determined using a colorimetric assay (GPO-Trinder). Western blotting was used to investigate the TNFα-induced phosphorylation of MAPK and perilipin expression. Fatcake and cytosolic fractions were prepared to examine the isoproterenol-stimulated hormone-sensitive lipase translocation. RESULTS: Treatment with curcumin attenuated TNFα-mediated lipolysis by suppressing phosphorylation of extracellular signal-related kinase 1/2 (ERK1/2) and reversing the downregulation of perilipin protein in TNFα-stimulated adipocytes (p<0.05). The acute lipolytic response to adrenergic stimulation of isoproterenol was also restricted by curcumin (10-20 µM, p<0.05), which was compatible with reduced perilipin phosphorylation(29%, p<0.05) and hormone-sensitive lipase translocation(20%, p<0.05). CONCLUSIONS: This study provides evidence that curcumin acts on adipocytes to suppress the lipolysis response to TNFα and catecholamines. The antilipolytic effect could be a cellular basis for curcumin decreasing plasma FFA levels and improving insulin sensitivity.

The association between GJB2 gene polymorphism and psoriasis: a verification study.

Psoriasis is a chronic inflammatory skin disease with multifactorial etiology. Connexin 26 (Cx26), an important gap junction protein, has been found highly expressed in plaques of psoriasis. Recently, genome wide association studies (GWAS) identified one new single nucleotide polymorphism (SNP) in GJB2 gene coding for Cx26 protein associated with psoriasis in Chinese Han population. In this paper, we verified the GWAS data in Chinese Han population. Here we genotyped the polymorphism of GJB2 rs3751385:C>T in 371 psoriasis patients and 330 healthy controls in Chinese Han population using polymerase chain reaction restriction fragment length polymorphism assay (PCR-RFLP). Our case-control assay indicated decreased frequency of the GJB2 rs3751385 C allele in psoriasis patients compared with that in the healthy controls [p = 6.02 × 10(-5), Odds ratio (OR) = 0.793, 95 % confidence interval (CI) 0.706-0.889]. The result suggested that GJB2 gene polymorphism rs3751385:C>T was associated with psoriasis susceptibility of Chinese Han population.

Overexpression of Insig-1 protects ß cell against glucolipotoxicity via SREBP-1c.

BACKGROUND: High glucose induced lipid synthesis leads to ß cell glucolipotoxicity. Sterol regulatory element binding protein-1c (SREBP-1c) is reported to be partially involved in this process. Insulin induced gene-1 (Insig-1) is an important upstream regulator of Insig-1-SREBPs cleavage activating protein (SCAP)-SREBP-1c pathway. Insig-1 effectively blocks the transcription of SREBP-1c, preventing the activation of the genes for lipid biosynthesis. In this study, we aimed to investigate whether Insig-1 protects ß cells against glucolipotoxicity. METHODS: An Insig-1 stable cell line was generated by overexpression of Insig-1 in INS-1 cells. The expression of Insig-1 was evaluated by RT-PCR and Western blotting, then, cells were then treated with standard (11.2 mM) or high (25.0 mM) glucose for 0 h, 24 h and 72 h. Cell viability, apoptosis, glucose stimulated insulin secretion (GSIS), lipid metabolism and mRNA expression of insulin secretion relevant genes such as IRS-2, PDX-1, GLUT-2, Insulin and UCP-2 were evaluated. RESULTS: We found that Insig-1 suppressed the high glucose induced SREBP-1c mRNA and protein expression. Our results also showed that Insig-1 overexpression protected ß cells from ER stress-induced apoptosis by regulating the proteins expressed in the IRE1α pathway, such as p-IRE1α, p-JNK, CHOP and BCL-2. In addition, Insig-1 up-regulated the expression of IRS-2, PDX-1, GLUT-2 and Insulin, down-regulated the expression of UCP-2 and improved glucose stimulated insulin secretion (GSIS). Finally, we found that Insig-1 inhibited the lipid accumulation and free fatty acid (FFA) synthesis in a time-dependent manner. CONCLUSIONS: There results suggest that Insig-1 may play a critical role in protecting ß cells against glucolipotoxicity by regulating the expression of SREBP-1c.

Rosiglitazone inhibits high glucose-induced apoptosis in human umbilical vein endothelial cells through the PI3K/Akt/eNOS pathway.

Previous studies have shown that the phosphatidylinositol 3-kinase / Akt / endothelial nitric oxide synthase / NO (PI3K/Akt/eNOS/NO) pathway is involved in high glucose-induced endothelial cell apoptosis and rosiglitazone has a protective effect on endothelium. In the present study, we investigated the antiapoptotic effect of rosiglitazone on human umbilical vein endothelial cells (HUVECs) exposed to high glucose and explored its possible mechanism. Treatment of high glucose (33 mmol/L) for 48 h significantly induced the apoptosis of HUVECs, concomitantly with increased caspase-3 activity. High glucose treatment also decreased Akt and eNOS phosphorylation levels with subsequent NO production. All these alterations induced by high glucose were attenuated by rosiglitazone (1 micromol/L). Interestingly, the antiapoptotic effect of rosiglitazone was inhibited by PI3K inhibitor (LY294002, wortmannin) or eNOS inhibitor NG-l-nitro-arginine methyl ester (l-NAME). The reverse effects of rosiglitazone on phosphorylation of Akt and eNOS with subsequent NO production were also inhibited by LY294002, wortmannin or l-NAME, respectively. These findings suggest that rosiglitazone inhibits high glucose-induced apoptosis in HUVECs through the PI3K/Akt/eNOS pathway.

[PI3K p85alpha expression and its role in the progression of colorectal cancer].

OBJECTIVE: To investigate the expression of PI3K p85alpha in normal colorectal tissue, colorectal adenoma and primary colorectal carcinoma and explore its significance in the progression of colorectal cancer. METHODS: The expression of PI3K p85alpha was detected in 116 normal colorectal tissue, colorectal adenoma and primary colorectal carcinoma specimens using immunohistochemical staining, and the relationship between the expression of PI3K p85alpha protein and the clinicopathological factors was analyzed. RESULTS: The positivity rates of the expression of PI3K p85alpha protein increased gradually in the progression of colorectal cancer and showed significant differences between the tissues (P<0.05). A significant difference was also noted in the positivity rates of the PI3K p85alpha expression in colorectal carcinoma tissues at different Dukes' stages (P<0.05). No obvious correlation was found between PI3K p85alpha expression and the degree of the tumor differentiation. CONCLUSIONS: Abnormal PI3K p85alpha expression occurs in the progression of colorectal cancer in close relation to the clinical stage, and the PI3K/AKT pathway plays an important role in the progression of colorectal cancer.

[Hyperlipidemia induced by high fat diet ingestion activates TGF-beta/Smad signaling pathway in the kidney of diabetic rats].

OBJECTIVE: To investigate the effect of diet-induced hyperlipidemia on TGF-beta/Smad signaling pathway in the kidney of diabetic rats, and to explore the mechanism by which hyperlipidemia leads to renal injury in diabetes. METHODS: Diabetic rats and non-diabetic rats were fed with normal fat diet and high fat diet for 16 weeks, respectively. The expressions of TGF-beta1, TbetaRII, and Col-IV mRNA in the renal cortex were examined by reverse transcriptase-PCR,TbetaRII and p-Smad staining in glomerular cells were detected by immunohistochemical staining, and the expression of TGF-beta1 and Col-IV protein was determined by Western blot. RESULTS: Diet-induced hyperlipidemia up-regulated the levels of TGF-beta1, TbetaRII, p-Smad, and Col-IV protein and mRNA in the renal cortex of diabetic rats compared with those of non-diabetic rats. However, feeding high fat diet to non-diabetic rats had no influence on the expression of TGF-beta1, TbetaRII, p-Smad2, and Col-IV in the renal cortex. CONCLUSION: Hyperlipidemia induced by high fat diet ingestion leads to renal injury in diabetic rats through activating TGF-beta1 /Smad signaling pathway.

Downregulation of secretory leukocyte proteinase inhibitor in chronic obstructive lung disease: the role of TGF-beta/Smads signaling pathways.

BACKGROUND: Secretory leukocyte proteinase inhibitor (SLPI) is an important antileukoprotease in airway. The aim of the present study was to explore the expression of SLPI in the bronchi and lung tissues of chronic obstructive pulmonary disease (COPD) models and the regulative mechanism by transforming growth factor (TGF)beta(1)/Smads signal pathway in bronchial epithelial cell. METHODS: COPD rat model was established and was treated with or without TGFbeta1 monoclonal antibody. Spirometry was conducted, and expressions of TGFbeta(1), Smad4 and SLPI were examined by immunohistochemistry and reverse-transcription polymerase chain reaction (RT-PCR), respectively. The normal human bronchial epithelial cell (NHBE) was cultured, preincubated with or without siRNA (Smad4), and then stimulated with TGFbeta(1). Expressions of Smad4 and SLPI were detected by immunocytochemistry, Western blot and RT-PCR, respectively. RESULTS: As compared with the model group, after treatment with TGFbeta(1) monoclonal antibody, peak expiratory flow (PEF), forced expiratory volume in 0.3 sec (FEV(0.3)) and FEV(0.3)/forced vital capacity (FVC) in the TGFbeta(1) monoclonal antibody intervention group were all significantly improved. Expression of SLPI was also improved, but expression of Smad4 was significantly decreased. Expression of SLPI in NHBE cells was inhibited by TGFbeta(1) both at the mRNA level and the protein level. Furthermore, effect of TGFbeta(1)-inhibited expression of SLPI in NHBE cells was disengaged by siRNA (Smad4) both at the mRNA level and the protein level. CONCLUSIONS: Decreased expression of SLPI in the COPD rat model may be mainly caused by the increased expression of TGFbeta(1), and this process is probably related to the activation of Smads signal pathway.

Palmitic and linoleic acids impair endothelial progenitor cells by inhibition of Akt/eNOS pathway.

BACKGROUND: Endothelial progenitor cells (EPCs) are involved in adult neovasculogenesis and maintenance of vascular integrity. Scarce data have been provided for the individual effect of elevated free fatty acids (FFAs) on EPCs. This study was designed to investigate the association between Akt/eNOS signal pathway changes and the proliferation/function of EPCs in the presence of palmitic and linoleic acids. METHODS: After 14-day culture, EPCs were stimulated with different concentrations of palmitic and linoleic acids, with or without SNP, L-NAME, or LY294002. The proliferation and ability of adhesion, migration and tube structure formation of EPCs were observed and the level of phosphorylated Akt protein expression and eNOS protein expression were assayed. RESULTS: Incubation with palmitic and linoleic acids at concentrations of 0.2 muM or higher inhibited EPCs proliferation, significantly reduced migratory rate, reduced adhesion to fibronectin and impaired ability of EPCs to form tube structure in a dose-dependent manner. A simultaneous dose-dependent NO generation and Akt phosphorylation decrease as well as eNOS expression reduction at protein levels were also observed. However, all of the detrimental effects were attenuated by pretreating EPCs with SNP, NO donor. AKT and eNOS inhibitor, LY294002 and L-NAME, respectively, augmented palmitic and linoleic acids inhibitory effects on EPCs. CONCLUSIONS: These findings suggest that palmitic and linoleic acids downregulated AKT/eNOS signal pathway, which contributed to overall poor function and decrease proliferation of EPCs. These changes induced by palmitic and linoleic acids in signaling offer a novel explanation for the overall poor function of EPCs in diabetes mellitus.

[Effect of rosiglitazone on NO and eNOS via PI3K/PKB signal pathways in cultured human umbilical vein endothelial cells].

OBJECTIVE: To observe the effect of rosiglitazone on the production of nitric oxide (NO) and the expression of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (PKB) /the endothelial nitric oxide synthase (eNOS) in cultured human umbilical vein endothelial cells(HUVECs), and to investigate the mechanism of signal transduction of rosiglitazone in improving the endothelial function. METHODS: HUVECs were treated with various concentrations of rosiglitazone. The NO level was measured using Griess Reaction in cell culture supernatants; the expressions of PI3K-, PKB- and eNOS mRNA were measured using RT-PCR; and the expressions of PKB, eNOS, and phosphorylation of PKB-Ser473, eNOS-Ser1177 were measured using Western Blot. RESULTS: Rosiglitazone increased the endothelial NO production in a dose- and time-dependent manner in cultured HUVECs, and also increased the expression of PI3K mRNA and the phosphorylation of PKB-Ser473 and eNOS-Ser1177 in a concentration-dependent manner, with no alteration in the expression of PKB and eNOS in cultured HUVECs. N(w)-nitro-L- arginine methyl ester (L-NAME, eNOS synthase inhibitor) blocked the rosiglitazone-induced NO formation; LY294002 (a PI3K inhibitor) prevented the NO production; and the phosphorylation of eNOS and PKB was induced by rosiglitazone. CONCLUSION: Treatment with rosiglitazone can increase the NO production and improve the endothelial function through up-regulating the PI3K/PKB/eNOS signal pathways in cultured HUVECs.

Metabolic syndrome among ethnic South Asian patients with ischemic stroke and comparison with ethnic Chinese patients: the Singapore General Hospital experience.

BACKGROUND: South Asians are the largest ethnic group in the world, yet there are no data on metabolic syndrome (MetS) among ethnic South Asian patients with ischemic stroke. Ethnic differences in the prevalence of MetS are known to exist. METHODS: We studied 126 consecutive ethnic South Asian patients and 126 age-, sex-, and diabetes-matched ethnic Chinese patients admitted with acute ischemic stroke. RESULTS: The prevalence of MetS among ethnic South Asian patients, at 61%, was significantly higher than among ethnic Chinese patients (47%) (P < .001). Of note, mean high-density lipoprotein was lower among ethnic South Asian compared with ethnic Chinese patients (P = .002). CONCLUSION: We describe a high burden of MetS among ethnic South Asian patients, which was significantly greater than that found among ethnic Chinese patients.

[Aortic endothelium-dependent vasodilation function and PI3K-, PKB-, eNOS mRNA expressions in insulin-resistant and type 2 diabetic rats].

OBJECTIVE: To observe the changes of aortic endothelium-dependent vasodilation function (EDVR) and expressions of endothelial nitric oxide synthase (eNOS), phosphatidylinositol 3-kinase (PI3K), and protein kinase B (PKB) in insulin-resistance (IR) and type 2 diabetic rats. METHODS: IR rat model was established by feeding 4-6 week-old male SD rats with high glucose and cholesterol diet for 6 weeks and type 2 diabetes (DM) were induced by intraperitoneal injection with low dose streptozotocin (STZ) to IR rats. Glucose infusion rate (GIR) was determined by euglycemic hyperinsulinemic clamp technique, EDVR by acetylcholine (Ach)-induced vasodilation response in isolated aortic rings, aortic NO concentration by Griess Reaction, activation of eNOS detected by immunohistochemical SP method, mRNA expressions of eNOS-, PI3K- and PKB of aorta were assayed by RT-PCR, aorta ultrastructure observed by electron microscopy. Body weight, fast plasma glucose (FPG), insulin (FINS), triglyceride (TG), cholesterol (TC) were determined and the insulin sensitivity index (ISI) was calculated. RESULTS: (1) Body weight, FINS, TG and TC levels were significantly higher while ISI and GIR significantly lower in IR and DM rats than that in normal control rats (P < 0.05). (2) Aorta EDVR decreased significantly in IR and DM group compared with that in control group (P < 0.05) and EDVR was also significantly reduced in DM rats than that in IR rats (P < 0.05). The maximum Ach-induced vasodilation response (EDVR(max), P < 0.01) was positively correlated with ISI and negatively correlated with FPG, TG, TC and FINS (P < 0.01). (3) Aortic NO concentration, the mRNA expressions of eNOS-, PI3K-, and PKB and eNOS immunohistochemical expression in aorta were significantly lower in IR and DM rats compared with normal control rats and the decrease was more pronounced in DM rats (P < 0.05 vs. IR). (4) Pathologic aortic ultrastructure changes were also visualized in IR and DM rats. CONCLUSION: Our results suggest that reduced NO concentration and expression as well as reduced PI3K-, PKB-, and eNOS mRNA expressions might contributed to the reduced EDVR function and related pathological ultrastructure changes in IR and DM rats.