Objective To investigate the role of inflammatory factors like serumleptin, adiponectin,interleukin-6( IL-6) , and C-reactive protein ( CRP) in the systemic inflammatory response of smokinginduced COPD. Methods Thirty male Wistar rats were randomly divided into three groups, ie. a high-dose smoking group, a low-dose smoking group, and a control group. Serum leptin, adiponectin, IL-6, and CRP levels were measured by ABC-ELISA. Results The serum leptin and adiponectin levels in both smoking groups decreased significantly compared with the control group( P lt; 0. 05) , while the difference was not significant between the two smoking groups ( P gt; 0. 05) . The serum IL-6 and CRP levels in both smoking groups increased significantly compared with the control group( P lt; 0. 05) , which were higher in the highdosesmoking group than those in the low-dose smoking group( P lt;0. 05) . Conclusions Smoking increases the serum levels of IL-6 and CRP, but reduces the serum levels of leptin and adiponectin in rats. These results suggest that leptin, adiponectin, IL-6, and CRP may be involved in the systemic inflammatory response of smoking-induced COPD.
Objective To investigate the effect of adiponectin on proliferation of airway smooth muscle cells( ASMCs) , and explore its possible mechanism. Methods ASMCs were derived fromrat airway tissue and were cultured in vitro. RT-PCR was used to verify the expression of adiponectin receptors on ASMCs. Then ASMCs were treated with adiponectin at different concentrations( 5, 10, 20, 40, 80 μg/mL) for different periods of time( 1, 12, 24, 48, 72 hours) , respectively. The absorbsence ratios of adiponectin at different concentrations were determined by MTT assay. The adenosine monophosphate-activated protein kinase( AMPK) and phosphorylated AMPK( pho-AMPK) in ASMCs were quantified by Western blot after being treated with adiponectin at different concentrations ( 5, 10, 20, 40 μg/mL) for 48 hours. ResultsThe inhibition of adiponectin on ASMCs was showed in dose-dependent manner( r = 0. 324, P lt; 0. 01) and time-dependent manner( r = 0. 607, P lt; 0. 05) . Western blot indicated that the expression of pho-AMPK increased with the increased concentrations of adiponectin( r =0. 607, P lt; 0. 01) . The ratio of pho-AMPK/AMPK were ( 27. 66 ±1. 03) % , ( 31. 91 ±0. 86 ) %, ( 75. 52 ±2. 67) % , and ( 84. 50 ±1. 05) % ,respectively, with significant differences between each concentrations of adiponectin( P lt; 0. 05) . There was no expression of pho-AMPK in the control group. Conclusion Adiponectin can significantly inhibit ASMCs’proliferation by activating AMPK.
【Abstract】 Objective To observe the plasma levels of adiponectin and interleukin-17 ( IL-17) in patients with chronic obstructive pulmonary disease ( COPD) at acute exacerbation or stable stage, and analyze their relationship. Methods Sixty male COPD patients with normal weight ( with BMI range of 18. 5-24. 9 kg/m2 ) were enrolled, including 30 patients with acute exacerbations of COPD ( AECOPD) and 30 patients with stable COPD. Twenty healthy nonsmoking male volunteers were included as controls. The plasma levels of adiponectin and IL-17 as well as lung function ( FEV1% pred and RV% pred) were measured in all subjects. Results The concentrations of adiponectin and IL-17 were significantly higher in the AECOPD patients than those of the patients with stable COPD and the contro1s ( P lt; 0. 001) . Theconcentrations of adiponectin and IL-17 were significantly higher in the patients with stable COPD than those of the controls ( P lt;0. 01) . Adiponectin was positively correlated with IL-17 in the AECOPD patients ( r =0. 822, P lt;0. 001) and in the patients with stable COPD ( r =0. 732, P lt;0. 001) . Adiponectin was positivelycorrelated with RV% pred in the AECOPD patients ( rs = 0. 764, P lt;0. 001) and in the patients with stable COPD ( rs =0. 967, P lt;0. 001) . There was no significant relationship between adiponectin and FEV1% pred ( P gt;0. 05) . Conclusions The plasma level of adiponectin in COPD patients is elevated which is relatedwith excessive inflation of lung. Adiponectin may be involved in the process of inflammation in COPD as a new pro-inflammatory cytokine.
Objective To comprehend the pathological features and possible pathogenesis of avascular necrosis of the femoral head (ANFH) by morphology and immunohistochemical observation of osterix (OSX) and adiponectin through in vitro traumatic and non-traumatic ANFH specimens, so as to provide a theoretical basis for cl inical treatment. Methods Sixty-six ANFH specimens were collected from 66 cl inical cases undergoing hip replacement surgery. Twenty-four cases of traumatic ANFH (group A) included 17 males and 7 females, aged 21 to 70 years with an average of 56.5 years; 23 cases of steroid-induced ANFH (group B) included 16 males and 7 females, aged 56 to 72 years with an average of 61 years; and 19 cases of alcohol ic ANFH (group C) were males, aged 55 to 67 years with an average of 58.5 years. Bone tissue was got from weight-bearing and non-weight-bearing area of the femoral head respectively. The basic pathological changes was observed by HE staining under the optical microscope, and the percentage of empty bone lacuna and the percentage of trabecular bone area were calculated. The morphological changes of ANFH in different groups were observedby scanning electron microscope (SEM). OSX and adiponectin expression were detected by immunohistochemical technique. Results Gross of the femoral head surface in each group was rough, collapse, articular cartilage loss, osteophyte formation; cross section: dark red in group A, and yellow in groups B and C. HE staining showed that weight-bearing area of ANFH have similar morphological features in three groups. In non-weight-bearing area of groups B and C, the fat cells in bone marrow markedly increased and were hypertrophic; however there were more fibrous tissue in group A. There were statistically significant differences (P lt; 0.001) in the percentage of empty bone lacuna of the weight-bearing and non-weight-bearing area among three groups. There were no statistically significant differences (P gt; 0.05) in the percentage of trabecular bone area among three groups. The SEM observation showed that three groups had similar pathological changes. Brown granules for OSX and adiponectin positive substance were mainly located in the osteoblast of bone marrow of the femoral head. There was statistically significant difference (P lt; 0.05) in the average absorbency (A) value of OSX between group A and groups B, C, but there was no statistically significant difference (P gt; 0.05) between groups B and C. While there was no statistically significant difference (P gt; 0.05) in the A value of adiponectin among three groups. Conclusion Hormones and alcohol necrosis have more obviously fatty degeneration, but the repair capacity of traumatic femoral head necrosis is ber than that of hormones and alcohol necrosis. Alcohol and hormones have inhibitory action on the OSX-mediated osteogenic differentiation. Hormones and alcohol may not affect osteoblast expressing adiponectin and its receptors.
Objective To evaluate the relationship between the single nucleotide polymorphisms (SNPs) of the adiponectin gene +45 in exon 2 and type 2 diabetes mellitus (T2DM) in Chinese population via meta-analysis. Methods Databases including PubMed, Ovid, CBM, VIP, CNKI, and WanFang Data were searched from inception to June 2012, and the references of articles were also retrieved to collect case-control studies about the correlation of SNPs of the adiponectin gene +45 in exon 2 and T2DM in Chinese population. According to the self-designed inclusion and exclusion criteria, two reviewers screened articles, extracted data, and assessed the quality of the included studies independently. Then meta-analysis was performed STATA 11.0, with stability evaluated by both stratified analysis and sensitivity analysis. Moreover, Begg’s funnel plot and Egger’s method were used to assess the published bias of articles. Results 21 articles involving 22 studies were included (3272 T2DM cases and 2597 controls). There were significant differences between the two groups in dominant, recessive and addictive genetic models, and the pooled ORs (95% CI) were 1.36 (1.04, 1.78), 2.07 (1.55, 2.75), and 2.44 (1.59, 3.75), respectively. Conclusion The genetic single nucleotide polymorphisms of the adiponectin +45 in exon 2 is associated with type 2 diabetes in Chinese population. G allele of APM1 is a risk factor for type 2 diabetes, no matter in dominant, recessive or addictive genetic models.
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.
Myocardial remodeling is a common pathological physiology change for a variety of heart diseases under stimulation such as stress or ischemia. The engine body will release a lot of cytokines to promote the change of myocardial structure and ultimately lead to heart failure. Myocardial remodeling includes myocardial cells remodeling and the extracellular matrix remodeling. In recent years, we find that the function of adipose tissue is not only about energy storage, buffering to protect, supporting and filling, but also has a powerful function of secretion. Adipose tissue can secrete various adipocytokines, such as leptin, adiponectin, visfatin, omentin, angiotensin Ⅱ, and so on. Current studies have shown that adipocytokines and myocardial remodeling are intimated. And this article will summarize the function of adipocytokines on myocardial remodeling.
The exact pathophysiological mechanisms of diabetic retinopathy (DR) remain elusive. The inflammatory reaction, retinal vascular leakage and retinal neovascularization are main features of DR. Adiponectin (APN) is an endogenous biological active protein secreted by adipocytes. It can increase insulin sensitivity, regulate blood glucose and lipid metabolism, and has anti-inflammation and anti-neovascularization functions. It may be involved in the development of DR. This review summarized the studies on the association between APN and DR in recent years.
Diabetic retinopathy (DR) is one of common and specific microvascular complications caused by diabetic mellitus, and remains a serious and common ocular complication leading preventable blindness. At present, the specific pathogenesis of DR is not completely clear, and many factors are involved in its occurrence and development. Adiponectin (APN) is an endogenous cytokine secreted by adipocytes. It is expressed in all layers of retina, especially in the outer layer (rods and cones). It is involved in regulating fatty acid oxidation and glucose metabolism by binding with specific receptors. In recent years, a lot of studies have found that APN can be involved in regulating blood glucose, inhibiting neovascularization, reducing inflammation, dilating blood vessels and improving vascular endothelial function. At present, the specific mechanism of APN in the occurrence and development of DR Remains to be determined. Further research on the level changes and the specific mechanism of action of APN in DR may help to identify the characteristic metabolic changes of DR, thus providing new biomarkers for the diagnosis of DR, while helping to promote the innovation of the treatment of DR.