Objective To investigate the role of vascular endothelial growth factor ( VEGF) in the pathogenesis of emphysema and its relationship with tumor necrosis factor alpha ( TNF-α) . Methods 48 rats were randomly divided into four groups, ie. a normal control group, an emphysema group, a rhTNFR∶Fc intervention group, and a sham intervention group. The rats in the emphysema group, the rhTNFR: Fc intervention group, and the shamintervention group were exposed to cigarette smoking for 80 days. After 30 days of exposure, rhTNFR: Fc hypodermic injection was administered in the rhTNFR: Fc intervention group while placebo was injected in the sham intervention group as control. Lung tissue sections were stained by hematoxylin and eosin. Mean linear intercept ( MLI) and mean alveolar numbers ( MAN) were measured to estimate the extent of emphysema. The level of TNF-αin serumand BALF, and the level of VEGF in BALF were measured with ELISA. Results In the emphysema group, MLI was higher and MAN was lower than those in the normal control group. Moreover, the levels of TNF-αin serum and BALF were higher, and thelevel of VEGF in BALF was lower significantly ( P lt;0. 05) . After the intervention with rhTNFR∶Fc, MAN increased and the serum TNF-αdecreased significantly compared with the emphysema group ( P lt; 0. 05) .However there were no significant differences in MLI, VEGF, and TNF-α in BALF ( P gt; 0. 05 ) . No correlation was found between the level of TNF-αand VEGF in BALF in the emphysema group. Conclusion VEGF and TNF-αare related to the pathogenesis of emphysema of smoking rats, and may contribute to the development of emphysema in different pathways.
Objective To investigate the changes of microRNA-150 ( miR-150) in peripheral blood leukocytes in sepsis patients, and their relationship with expression of immune cytokines and sepsis severity. Methods The level of mature miR-150 was quantified by real-time reverse transcriptase-polymerase chain reaction (RT-PCR) and normalized to that of control miRNA, U6, in peripheral blood leukocytes of 40 patients with sepsis, 20 patients with systemic inflammatory response syndrome ( SIRS) , and 20 normal individuals. Serum concentrations of tumor necrosis factor alpha (TNF-α) and interleukin-10 (IL-10) were measured by enzyme-linked immunoabsorbent assay in all subjects. The sequential organ failure assessment ( SOFA) score systemwas used to evaluate the severity of sepsis. The relationships between miR-150 and the white blood cell count ( WBC) , TNF-α, IL-10 and SOFA score of the sepsis patients were analyzed. Results MiR-150 was stable for at least 5 days when specimen stored at 4 ℃ and the determination of miR-150 had a broad linear detecting range ( 6. 97-6. 97 ×104 pg/ μL RNA, the lowest detecting limit: 6. 97 pg/μL RNA,r=0.999) .MiR-150 expression in the peripheral blood leukocytes in the sepsis group was significantly lower than that in the healthy control group ( Plt;0.01) , while WBC, IL-10 and IL-10/TNF-α ratio were significantly higher ( Plt;0.05) . There was no significant difference in levels of miR-150, IL-10, IL-10/TNF-α ratio, and WBC between the sepsis group and the SIRS group (Pgt;0.05) . There was no significant difference in serum concentrations of TNF-α among three groups ( Pgt;0.05) . MiR-150 expression in non-survivor sepsis patients was significantly lower than that in survivor sepsis patients (Plt;0.05) , while serum IL-10 and IL-10/TNF-αratio were significantly higher (Plt;0.01) , but there was no significant difference in serum TNF-α between the non-survivor group and the survivor group ( Pgt;0.05) . There was significantly negative correlation between miR-150 and SOFA score, TNF-α and IL-10( r=-0. 619, - 0.457, -0. 431, Plt;0.05, respectively) , but no correlation between miR-150 and WBC ( r =-0. 184, Pgt;0.05) . There was no relationship between serum TNF-α, IL-10, IL-10 /TNF-α ratio or SOFA score ( Pgt;0.05) . Conclusions MiR-150 expression in the peripheral blood specimens is significantly decreased in sepsis patients. The expression level of miR-150 not only reflect the situation of inflammatory response, but also may be used as a prognostic marker in sepsis, as it can reflect the severity of sepsis in certain degree.
Objective To measure the serum level of adiponectin and explore its clinical implication in patients with asthma in acute exacerbation and remission phase. Methods 97 patients with asthma were recruited, including 50 patients with asthma in acute exacerbation and 47 patients in remission phase fromOctober 2010 to September 2011. 27 healthy nonsmoking volunteers of normal weight ( BMI range of 18.5-24. 9 kg/m2 ) were included as control. The concentrations of adiponectin and tumor necrosis factor alpha ( TNF-α) in serum were measured by enzyme-linked immunosorbent assay ( ELISA) . The lung function was tested in all subjects. The correlations between adiponectin, TNF-αand lung function were investigated. The data was analyzed using SPSS 19. 0 software. Variables were compared with one-way ANOVA. The correlations between variables were analyzed using Peason’s correlation coefficient or Spearman correlation coefficient.Results Serum adiponectin level was significantly lower in the patients with asthma in acute exacerbation [ ( 246 ±1. 21) ng/mL] than that in the healthy subjects [ ( 9. 64 ±4. 88)ng/mL] and the patients in remission phase [ ( 3. 79 ±0. 96) ng/mL] ( P lt; 0. 01) , while serum adiponectin level was also significantly lower in the patients in asthma remission phase than that in the healthy subjects ( P lt; 0. 01) . The serum adiponectin level in the patients with asthma in acute exacerbation or in asthma remission phase was negatively correlated with the serum TNF-α level ( P lt; 0. 01) , and was positively correlated with FEV1 /predicted value ( P lt; 0. 01) . Conclusions The serum adiponectin is reduced in asthma patients and may play a protective role in asthma.
ObjectiveTo explore the levels of serum leptin,TNF-α,IL-8 and hypersensitivity C-reactive protein (hs-CRP) in stable COPD patients with different body mass index (BMI). Methods30 healthy controls with BMI 18.5 to 23.9 kg/m2 and 105 patients with stable COPD were recruited in the study. The serum levels of leptin,TNF-α,and IL-8 were determined by radioimmunoassay and hs-CRP level was determined by versatile biochemical automatic analyzer. The COPD patients were divided into a low BMI group (BMI<18.5 kg/m2,n=32),a normal BMI group (BMI 18.5-23.9 kg/m2,n=48),and a high BMI group (BMI≥23.9 kg/m2,n=25). ResultsSerum leptin level in the COPD patients was significantly reduced compared with the control subjects (P<0.05). Serum leptin levels were reduced in the low BMI and the high BMI groups compare with the normal BMI group [(7.89±3.16)ng/L and (10.52±5.98)ng/L vs. (13.04±5.73) ng/L,P<0.01 or P<0.05]. Leptin level in the low BMI group was lower than that in the high BMI group (P<0.05). Serum TNF-α levels were significantly increased in the low BMI group compared with the normal BMI and high BMI groups [(229.39±89.57)μg/L vs. (180.06±74.24) μg/L and (189.46±82.41) μg/L,P<0.01]. Serum TNF-α level in the COPD patients was significantly increased compared with the control subjects [(192.37±83.65) μg/L vs. (178.59±60.38) μg/L,P<0.05]. The IL-8 levels were not significant different among three BMI groups with COPD. The hs-CRP level in the high BMI group was higher than that in the low BMI and normal BMI groups (P<0.05). ConclusionLeptin and TNF-α may be involved in weight-loss of COPD malnutritional patients.
ObjectiveTo investigate the levels of nutritional status, serum leptin, TNF-α, IL-8 and C-reactive protein(CRP) in patients with two clinical phenotypes of COPD. MethodsNutritional parameters, including body mass index, percent ideal body weight, triceps skin-fold thickness, mid-upper arm circumference, albumin, lymphocytes count, serum leptin, TNF-α, IL-8 and CRP levels were determined in 40 healthy controls and 120 patients with COPD. The COPD patients were divided into a typical emphysema type(A group) and a bronchitis type(B group), both groups included COPD patients in acute exacerbation phase and in stable phase. ResultsThe nutritional parameters in B group were higher than those in A group(P < 0.05). Serum leptin level was lower in stable A group and stable B group than that in the control group[(7.76±2.93) ng/L and (10.04±5.11) ng/L vs. (14.93±8.47) ng/L, P < 0.05], higher in A group[(12.99±5.56) ng/L)] and B group in acute exacerbation phase[(13.52±5.82) ng/L] than that in stable phase(P < 0.05), and lower in stable A group than that in stable B group (P < 0.05). Serum TNF-αlevel was higher in A group with acute exacerbation than that in B group with acute exacerbation and the control group[(234.65±95.74)μg/L and(195.03±88.00)μg/L vs. (182.07±42.35)μg/L, P < 0.05], and higher in stable A group than that in stable B group[(225.31±84.14)μg/L vs. (188.17±72.62)μg/L, P < 0.05]. Serum IL-8 level in A and B groups in acute exacerbation phase and stable phase was higher than that in the control group(P < 0.05), and was not significantly different between A group and B group in acute exacerbation or stable phase(P > 0.05). The CRP level was higher in A group and B group with acute exacerbation than that in the control group[(46.87±35.89) mg/L and(70.11±65.50) mg/L vs. (5.05±4.49) mg/L, P < 0.01], and higher in B group with acute exacerbation than that in A group with acute exacerbation (P < 0.05). ConclusionsThere are differences in nutritional status, serum leptin, TNF-αand CRP levels between the emphysema type and bronchitis type of COPD, while the IL-8 level is not different between two phenotypes. Leptin and TNF-αmay be involved in weight-loss of malnutritional COPD patients.