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Increased body weight affects the whole body including the immune response, and leads to a state of non-specificinflammation, which leads to increased incidence of inflammatory diseases. The aim of this study was to determine therelationship between adiposity and the hematological profile, and serum concentrations of glucose, C-reactive protein(CRP), some pro-inflammatory [leptin, resistin, interlukin-6 (IL-6), and tumor necrosis factor alpha (TNF-α)] and antiinflammatory (adiponectin) adipokines in 112 healthy Saudi female university students. Adiposity was determined using thebody mass index (BMI), waist-to-hip ratio (WHR), and waist circumference (WC). The results showed that the mean totalwhite blood cell counts were significantly higher for the high risk WHR group, and the mean platelet and red blood cellcounts were higher for the obese/morbidly obese BMI group compared to the respective controls. The white blood cell typesand hemoglobin did not show any significant differences. Mean serum CRP, leptin, resistin, and IL-6 concentrations weresignificantly higher for the obese/morbidly obese BMI and high risk WC subjects compared to the healthy weight subjects.The only significant difference for the WHR groups was a significantly higher mean resistin level for the moderate riskgroup compared to the control. Mean glucose, TNF-α and adiponectin concentrations were not significantly different amongthe groups. Thus, it may be concluded that the immune system cells and the hematological profile in subjects with highadiposity were minimally affected compared to the healthy weight subjects. They also had higher platelet counts, and CRP,leptin, resistin, and IL-6 concentrations, which are inflammatory effectors/markers, thus confirming that obese subjects hadheightened inflammation and a higher risk for inflammatory diseases.
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Objective To study the mechanism of IL-6 stimulated the secretion of IL-10 in nasopharyngeal carcinoma CNE-2 cells.Methods Nasopharyngeal carcinoma CNE-2 cells were cultured with recombination cytokine IL-6 in vitro,or anti-IL-6 receptor antibody and signal pathway inhibitor were pre-incubated for 1 hour,and then IL-6 were added,the mRNA and protein level of IL-10 were separately detected by RT-PCR and enzyme-linked immunosorbent assay.Results Compared with the control group,the expression and secretion of IL-10 in IL-6 stimulated group were significantly increased,which was in a dose and time dependent way,the difference was significant(P ＜ 0.01).Additionally,IL-6 stimulated the expression and secretion of IL-10 by CNE-2 cells were significantly decreased in following pre-incubated with anti-IL-6 receptor antibody or NF-κB inhibitor,the difference was significant(P ＜ 0.01),but such effect was not detected when CNE-2 cells were pre-incubated with the PI3K inhibitor,p38/MAPK inhibitor,JNK inhibitor,MEK1/2 inhibitor and STAT3 inhibitor.Conclusion IL-6 can induce the expression and secretion of IL-10 in nasopharyngeal carcinoma CNE-2 cells via IL-6R/NF-κB signal pathway,and blocking IL-6 signal may be useful for the immunotherapy of nasopharyngeal carcinoma.
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Background : Polycystic ovarian syndrome (PCOS) is a low-grade inflammatory disease characterized by hyperandrogenemia, hirsutism, chronic anovulation and vascular disorder. Interleukin-6 (IL-6), cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) are triggered by inflammatory stimuli and lead to angiogenesis and pathogenesis of the ovary. Honeybee venom (HBV) contains an array of biologically active components possessing various pharmaceutical properties. This study was designed to assess the possibility of HBV application as an anti-inflammatory therapeutic agent to suppress levels of the main inflammatory mediators IL-6, COX-2 and VEGF. To induce PCOS, 1 mg of estradiol valerate (EV) per 100 g of body weight was subcutaneously (SC) injected into eight-week-old rats. After 60 days, 0.5 mg/kg of HBV was administered Intraperitoneal (IP) for 14 consecutive days, and the results of PCOS treatment were investigated. Rats were then anesthetized with CO2, and the ovaries were surgically removed. Serum IL-6 was detected by the ELISA kit. Immunoexpression of COX-2 and VEGF were examined in three groups: EV-induced PCOS, HBV-treated PCOS and control animals. Results : Thickness of theca layer, number and diameter of cysts and levels of IL-6 significantly decreased in HBV group relative to PCOS group. The immunohistochemical analysis showed an increase in COX-2 and VEGF expression in PCOS group whereas HBV-treated rats presented weak and irregular immunostaining. Conclusions : Our results suggest that the beneficial effect of HBV may be mediated through its inhibitory effect on serum IL-6 level and ovarian COX-2 and VEGF expression.(AU)
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Animals , Ovary , Bee Venoms , Interleukin-6 , Rats, Wistar , Vascular Endothelial Growth Factor AABSTRACT
Background : Polycystic ovarian syndrome (PCOS) is a low-grade inflammatory disease characterized by hyperandrogenemia, hirsutism, chronic anovulation and vascular disorder. Interleukin-6 (IL-6), cyclooxygenase-2 (COX-2) and vascular endothelial growth factor (VEGF) are triggered by inflammatory stimuli and lead to angiogenesis and pathogenesis of the ovary. Honeybee venom (HBV) contains an array of biologically active components possessing various pharmaceutical properties. This study was designed to assess the possibility of HBV application as an anti-inflammatory therapeutic agent to suppress levels of the main inflammatory mediators IL-6, COX-2 and VEGF. To induce PCOS, 1 mg of estradiol valerate (EV) per 100 g of body weight was subcutaneously (SC) injected into eight-week-old rats. After 60 days, 0.5 mg/kg of HBV was administered Intraperitoneal (IP) for 14 consecutive days, and the results of PCOS treatment were investigated. Rats were then anesthetized with CO2, and the ovaries were surgically removed. Serum IL-6 was detected by the ELISA kit. Immunoexpression of COX-2 and VEGF were examined in three groups: EV-induced PCOS, HBV-treated PCOS and control animals. Results : Thickness of theca layer, number and diameter of cysts and levels of IL-6 significantly decreased in HBV group relative to PCOS group. The immunohistochemical analysis showed an increase in COX-2 and VEGF expression in PCOS group whereas HBV-treated rats presented weak and irregular immunostaining. Conclusions : Our results suggest that the beneficial effect of HBV may be mediated through its inhibitory effect on serum IL-6 level and ovarian COX-2 and VEGF expression.
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Objective To investigate the effect of rosmarinic acid on the behavioral changes in enhanced single prolonged stress (ESPS) model rats and the levels of interlukin-1β (IL-1β) and interlukin-6 (IL-6) in the hippocampus.Methods 48 adult male Sprague Dawley rats were randomly divided into six groups (n =8):Control group,Control + RA (L) group,Control + RA (H) group,ESPS group,ESPS + RA (L) group and ESPS + RA (H) group.Behavioral changes of these rats were analyzed by open field test and elevated plus-maze.The levels of IL-1 β and IL-6 were measured by enzyme linked immunosorbent assay (ELISA).Results (1) Open field test showed that the number of central region entering and the fraction of time exploring in center of ESPS group were significantly reduced than that of Control group ((18.13 ± 10.15) times,(26.68 ± 10.06) ％) and ESPS + RA (H) group ((16.88 ± 8.81) times,(25.08 ± 8.52) ％) (P ＜ 0.05).And it showed no significant difference among Control + RA(L) group,Control + RA(H) group and Control group.Meanwhile,there was also no statistic difference between ESPS group and ESPS + RA(L) group.(2) Elevated plus-maze test showed that percentages of open arm entries and fraction of time exploring in open arm in reference to total number of entries into all arms and total time spent on all arms in ESPS group were significantly reduced than that of Control group((37.38 ± 8.24)％,(17.63 ±4.74)％) and ESPS + RA(H) group((33.72 ±9.49)％,(16.99 ±4.28)％) (P ＜ 0.05),but there was no significant difference between that of ESPS group and ESPS + RA(L) group(P＞0.05).It also showed no significant difference among Control + RA (L) group,Control + RA (H) group and Control group.(3) Compared with ESPS group,RA(10mg/kg) reduced the levels of IL-1β and IL-6 in the hippocampus,but RA(5mg/kg) did not have this effect.(4) Correlation analysis results showed the level of IL-1β in the hippocampus was negatively related with the ameliorated PTSD-like behaviors of ESPS exposure rats.Conclusion RA can ameliorate PTSDlike behaviors of ESPS exposure rats,and this effect may be carried out by down-regulating the levels of IL-1β and IL-6 in the hippocampus,especially the IL-1β.
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Objective To observe the effect of rosiglitazone on the concentration of interlukin (IL)-6 and IL-10 in lung tissues of diabetic rats.Methods The experimental diabetic rats were yielded by injecting streptozotocin(STZ) and feeding with high fat and high glucose food.We observed lung morphology in control group,diabetes mellitus(DM) group,and rosiglitazone group at 10 week and 20 week respectively under light microscope.Alteration of IL-6 and IL-10 in lung was measured by immunohistochemistry.Results The optical density values of IL-6 in the control group,the DM group and the roggerosiglitazone treatment group were 0.15 ±0.01,0.16 ±0.01;0.22 ±0.02,0.31 ±0.04;0.22 ±0.03,and 0.20 ±0.02 at 10 week and 20 week respectively (Fwithin =216.89,P ＜ 0.01 ; Fbetween =342.62,P ＜ 0.01 ; Finteraction =341.51,P ＜ 0.01).Any two groups had significant difference(P ＜ 0.05) except the comparison of the IL-6 values at 10 week and 20 week in the control group (P ＞ 0.05).The absorbance values of IL-10 in the three groups were 0.13 ± 0.01,0.15 ±0.02;0.20 ±0.01,0.21 ±0.01;0.20 ±0.02,and 0.17 ±0.01 at 10 week and 20 week respectively (Fwithin =14.612,P ＜0.01 ;Fbetween =909.19,P ＜0.01 ;Finteraction =210.55,P ＜0.01).Any two groups had significant difference(P ＜0.05) except the comparison of the IL-6 values at 10 week and 20 week in the control group.Conclusion The elevated levels of IL-6 and IL-10 in lung tissue of dibtetic rats might be related to the inflammation of lung tissues.Rosiglitazone may alleviate lung inflammation by regulating the levels of IL-6 and IL-10.
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Objective To investigate the possible mechanisms of the attribution of psychological stress to the temporomandibular joint disorder(TMD) ,through the evaluation of the animal model and detection of the proinflammatory cytokines in the TMJ.Methods The animal models of communication box were built to mimic the psychological stress.The concentration of the serum Cor and ACTH was detected in the control group, Psychological Stress group ( PS group), and diazepam ( anti-anxiety drug) group ( PS + DI group).The expression of the proinflammatory cytokines IL-1 and IL-6 in the rat TMJ in the different phases of psychologicalstress was detected by RT-PCR.Results The results of the serum concen- tration of Cor and ACTH showed that there was significant difference between the control group and the PS group(P＜0.01 ) ,while no significant difference between the control group and the PS + DI group(P＞0.05).The expressions of IL-1 and IL-6 were comapared in all group.The expressions of IL-1 in CON group were (0.453± 0.021 ) mg/L, (0.439 ± 0.028 ) mg/L and (0.454 ± 0.023 )mg/L.These values were markedly increased compared with those of the PS group(0.981 ±0.024)mg/L, (0.746±0.017)mg/L and (0.510 ±0.016)mg/L respectively, P＜0.01 ) ,but no significant differences compared with PS + DI group(0.549 ± 0.014 ) mg/L, ( 0.498 ± 0.014 ) mg/L and ( 0.444 ± 0.022 ) mg/L respectively, P ＞ 0.05).Similar changes were observed in expressions of IL-6.The expressions of IL-6 in the CON rats were (0.525 ±0.028)mg/L,(0.515 ±0.028)mg/L and (0.518 ±0.022)mg/L,respectively,while those of PS group were(0.820 ± 0.023 ) mg/L, (0.694 ± 0.019 ) mg/L and (0.579 ± 0.015 ) mg/L, respectively, which were significan- tly higher in the PS groups(P＜ 0.05 ).But there were no significant differences between CON group and PS + DI group( (0.599 ±0.015)mg/L, (0.541 ±0.015)mg/L, (0.487 ±0.008)mg/L respectively, P＞0.05).Conclusion The psychological stress can play important role in the formation of TMD.
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Objective To discuss the clinical value of high-sensitivity C-Reactive protein ( hs-CRP) and Interlukin-6 (IL-6) on patients with diabetes mellitus and athero sclerosis. Methods Serum hs-CRP is measured through particle enhanced immuoturbidimetric method by using analysis instrument 7200 . LDL-C is examined by one-step method. IL-6 is measured by double antibody assay. Results (1) Diabetic with higer LDL-C: the density of serum hs-CRP is (6. 81 ?3. 32) mg/L. IL-6 is (17. 2 ?5. 6) mg/L . Both are remarkably positive related. related coefficient r = 0. 61 ;P 0. 05). Conclusion For diabetic serum IL-6 plays roles in inducing the synthetic of CRP when there is an acute liver and also plays roles in the pathologic process of diabetes athero sclerosis.
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Objective To test whether IL 6 has any harmful effects on developing brain in neonatal rats, and try to illustrate its probable pathogenesis. Methods The neonatal rats were injected with different doses of rhIL 6 intravenously or intraventricularly. Animals were killed at 24 or 48 hours after injection to observe the pathological changes of brain tissues. Results Among animals killed at 24 hours after the intravenous injection with 1 000 U or 5 000 U rhIL 6, perivascular edema and ischaemic changes of neurons appear in their brain. There is no difference in the pathological changes in the brain of the rats treated with different doses. 72 hours after the intravenous injection, edema is still obvious, and ischaemic cell change in neurons aggravates into homogenizing cell change. When the brains are examined at 24 hours after intraventricular injection with 1 000 U rhIL 6, the pathological changes are the same as those treated by intravenous injection. Subarachnoid hemorrhage occurs more frequently in animals examined at 24 hours after 5 000 U rhIL 6 intraventricular injection than in those with intravenous injection. Besides, there appears local demyelination in the brain examined at 72 hours after the intraventricular injection of 5 000 u rhIL 6. Conclusion IL 6 by intravenous injection and intraventricular injection has harmful effects on the brain of neonatal rats.
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AIM To explore the role of nitric oxide (NO) mediators in seizure behavior and the related expression of interlukin 6(IL 6). METHODS The IL 6 immunoreactivity (IL 6 ir) and behaviour were observed in kainic acid (KA) induced seizure following pretreatment with L nitroarginine( L NNA), a inhibitor of nitric oxide synthase(NOS), or the same number of moles of L arginine( L Arg). RESULTS The results showed that time dependent seizures were induced on animals after administration of KA (10 mg?kg -1 ), accompanied by the immediate enhancement of IL 6 ir in hippocampal structure, piriform area and cortex. The behaviors of rats were not markedly altered by chronic pretreatment with L NNA (50 mg?kg -1 ) or L Arg (40 mg?kg -1 ). However, after the administration of KA, the seizure behaviors were obviously different in the group of L NNA and L Arg respectively. Seizure was agrevated in the animals with L NNA pretreatment and many rats died at KA 3 hours, whereas seizure was alleviated after KA in the group of L Arg. IL 6 expression was apparently up regulated in some brain areas such as hippocampus in the group of KA pretreated with L NNA, but opposite effects appeared in the group pretreated with L Arg before KA injection. CONCLUSION These results indicate that endogenous NO mediators may alleviate the seizure behaviors and may down regulated the early expression of IL 6 in KA challenged seizure, but it the mechanism of the early expression of IL 6 with the homeostasis of endogenous NO mediator merits further study.nismoftheearlyexpressionofIL 6withthehome
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The aim of this study was to explored the mechanism of inhibitory effect of chloroquine on IL-6 release induced synergistically by bacterial DNA and endotoxin. Before experiment mice were sensitized for 1 hour with D-GalN by I.P. injection. Mortality within seven days was observed after mice were challenged with CpG ODN or LPS with or without chloroquine treatment. ANA-1 cell line cells were cultivated in vitro. We investigated the influence of chloroquine on IL-6 release induced by both EC DNA and LPS. Expressions of TLR4 and TLR9 and activation of NF-?B p65 were investigated in cultured THP-1 cells pretreated with chloroquine and stimulated by EC DNA and LPS. The results showed that all mice died within 4 hours after challenged with CpG ODN and LPS. Only 4 or 5 mice pretreated with chloroquine (30mg/kg) died after challenged with CpG ODN and LPS (P