Evaluation of adipokine chemerin in hypertensive obese / Avaliação da adipocina chemerin em obesos hipertensos

Chemerin is an adipokine secreted by adiopose tissue and has a role in obesity and hypertension. This study aims at assessing the level of the adipokine chemerin in obesity and/or hypertension and correlating its level with the inflammatory marker hs-CRP and predictors of atherosclerosis as lipid profile, insulin resistance, systolic (SBP) and diastolic blood pressure (DBP).Volunteers were divided into 4 equal groups according to body mass index (BMI) and blood pressure: normal weight group (BMI ≤ 24.9 kg/m2), overweight group (BMI = 25.0 ­ 29.9 kg/m2), normotensive obese group (BMI ≥ 30.0 kg/m2) and hypertensive obese group (BMI ≥ 30.0 kg/m2). Chemerin, high-sensitivity C-reactive protein (hs-CRP), lipid profile, fasting blood glucose (FBG) and fasting insulin (FI) were evaluated in the mentioned groups.The results showed that there were significant increases of chemerin, hs-CRP, low density lipoprotein (LDL), SBP and DBP in hypertensive obese group compared to normotensive obese , overweight and normal weight groups. Moreover the only significant positive correlation between chemerin and hs-CRP was observed in the obese hypertensive group. The normotensive obese group showed significant increases of hs-CRP, LDL, triglyceride (TG), FBG, FI and the homeostasis model assessment-insulin resistance index (HOMA-IR) compared to the overweight and normal weight groups. Regarding the overweight group, there were significant increases in chemerin, hs-CRP, cholesterol, LDL, TG compared to the normal weight group, while the HDL levels were significantly lower compared to the two obese groups. These results revealed that the pro-inflammatory adipokine chemerin increases in obesity associated with hypertension, leading to the suggestion that there is a definite dysregulation of the pro-inflammatory and anti-inflammatory parameters towards the pro-inflammatory when hypertension and obesity are associated.

A chemerin é uma adipocina secretada pelo tecido adiposo e tem papel na obesidade e na hipertensão. Este estudo tem como objetivo avaliar o nível da adipocina chemerina na obesidade e / ou hipertensão e correlacionar seu nível com o marcador inflamatório hs-PCR e os preditores de aterosclerose como perfil lipídico, resistência à insulina, pressão arterial sistólica (PAS) e diastólica (PAD) Os voluntários foram divididos em 4 grupos iguais de acordo com o índice de massa corporal (IMC) e pressão arterial: grupo com peso normal (IMC ≤ 24,9 kg / m2), grupo com sobrepeso (IMC = 25,0 - 29,9 kg / m2), grupo obeso normotenso (IMC ≥ 30,0 kg / m2) e grupo obeso hipertenso (IMC ≥ 30,0 kg / m2). Chemerin, proteína C-reativa de alta sensibilidade (PCR-as), perfil lipídico, glicemia de jejum (FBG) e insulina de jejum (FI) foram avaliados nos grupos mencionados. Os resultados mostraram que houve aumentos significativos de chemerina, hs- CRP, lipoproteína de baixa densidade (LDL), PAS e PAD no grupo obeso hipertenso em comparação com obesos normotensos, com sobrepeso e com peso normal. Além disso, a única correlação positiva significativa entre chemerin e hs-CRP foi observada no grupo de hipertensos obesos. O grupo obeso normotenso apresentou aumentos significativos de PCR-as, LDL, triglicérides (TG), FBG, FI e o modelo de avaliação da homeostase - índice de resistência à insulina (HOMA-IR) comparado aos grupos com sobrepeso e peso normal. Em relação ao grupo com excesso de peso, houve aumento significativo de chemerina, PCR-as, colesterol, LDL, TG em relação ao grupo com peso normal, enquanto os níveis de HDL foram significativamente menores em comparação aos dois grupos obesos. Esses resultados revelaram que a pró-inflamatória adipocina chemerina aumenta na obesidade associada à hipertensão, levando à sugestão de que há uma desregulação definida dos parâmetros pró-inflamatórios e anti-inflamatórios em relação ao pró-inflamatório quando a hipertensão e a obesidade estão associadas.

A polysaccharide purified from Radix Adenophorae promotes cell activation and pro-inflammatory cytokine production in murine RAW264.7 macrophages / 中国天然药物

Radix Adenophorae, a traditional Chinese medicine, has been reported to have a variety of biological functions. In the present study, a polysaccharide component, Radix Adenophorae Polysaccharide (RAPS), was purified from Radix Adenophorae by decoloring with ADS-7 macroporous adsorption resin, DEAE-52 cellulose ion-exchange chromatography, and Sephacryl S-300HR gel chromatography, with the purity of 98.3% and a molecular weight of 1.8 × 10(4) Da. The cell viability assay and microscopic examination revealed that RAPS promoted the proliferation and activation of macrophages. At 400 μg·mL(-1), RAPS stimulated RAW264.7 cell proliferation by 1.91-fold compared with the control. Meanwhile, RAPS significantly increased the secretion of pro-inflammatory cytokines (TNF-α and IL-6) in a dose-dependent manner in the supernatant of RAW264.7 cell culture as determined by ELISA. At 400 μg·mL(-1), the production of TNF-iα was 20.8-fold higher than that of the control. Simultaneously, the production of nitric oxide (NO) and the expression of inducible nitric oxide synthase (iNOS) were increased in RAW264.7 cells incubated with RAPS, as measured by Griess assay and Western blot analysis. The NO production of cells treated with RAPS (400 μg·mL(-1)) reached 15.8 μmol·L(-1), which was 30.4-fold higher than that of the control (0.53 μmol·L(-1)). These data suggested that RAPS may enhance the immune function and protect against exogenous pathogens by activating macrophages.

Fentanyl induced hyperalgesia and upregulation of pro-inflammatory cytokines in dorsal root ganglions in ;rats / 实用医学杂志

Objective To investigate the expression of pro-inflammatory cytokines in lumbar dorsal root ganglions (DRG) of rats model of high-dose fentanyl induced hyperalgesia. Methods 64 male SD rats were divided into 2 groups (n = 32), fentanyl group and normal saline (NS) group. The rats were injected with fentanyl (60 μg/kg) or NS 4 times in total subcutaneously with a 15-minute interval. Mechanical and thermal nociception were measured via the tail pressure test (tail flick thresholds, TFT) and paw withdrawal test (paw withdrawal latency, PWL) at 1 day before, at 1, 2, 3 and 4 hour and on 1 ~ 7 day after administration. 4 rats were sacrificed and the lumbar DRG were harvested to analyze the expression of PGE2 , IL-1β, IL-6 and TNF-αvia ELISA. Results There were no significant changes of TFT, PWL and the expression of pro-inflammatory cytokines in DRG compared to baseline of rats in NS group. The value of TFT , PWL in fentanyl group were above the baseline at the 1 ~ 4 hour and below the baseline at 1~3 day after fentanyl injections. PGE2 , IL-1β, TNF-α and IL-6 increased on 1,3,5,7 day after fentanyl injections significantly. Conclusions High-dose fentanyl induced significant hyperalgesia and up-regulation of pro-inflammatory cytokines in DRG. The expression pro-inflammatory cytokines peaked later and were more protracted than the change of behavior test and show no direct relationship between the two.

Molecule mechanisms of the pro-inflammatory cytokine's effect on intestinal epithelium tight junctions / 肠外与肠内营养

The pro-inflammation cytokine is secreted by cells,and the function is to promote and regulate inflammatory reactions.They include IL-1,IL-6,TNF-? and IFN-?.Researchs have revealed that the levels of serum pro-inflammation cytokinemight increase notably in inflammatory bowel disease patients and they could cause the change of intestinal epithelium tight junctions.