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ObjectiveTo investigate the application value of Qingre Huashi Sanjie enema prescription in the treatment of the patients with sequelae of pelvic inflammatory disease (syndrome of combined dampness,heat,and stasis) and the effects of this prescription on inflammatory mediators and T lymphocyte subsets. MethodThe patients with sequelae of pelvic inflammatory disease (syndrome of combined dampness,heat,and stasis) treated from May 2022 to August 2023 were included in this study and randomized into two groups (79 cases). The control group was treated with conventional Western medicine,and the observation group was treated with Qingre Huashi Sanjie enema prescription on the basis of the therapy in the control group. Both groups were treated for 12 weeks. The serum levels of monocyte chemoattractant protein-1 (MCP-1),transforming growth factor-β1 (TGF-β1),and interleukin-6 (IL-6) were measured by enzyme linked immunoserbent assay (ELISA) before and after treatment in both groups. The erythrocyte sedimentation rate (ESR) and fibrinogen (FIB) were measured by an automatic blood rheology analyzer before and after treatment in both groups. The serum levels of CD4+,CD4+/CD8+ before and after treatment in both groups were measured by flow cytometry. The traditional Chinese medicine (TCM) symptom score and the 36-item short form survey (SF-36) score were assessed before and after treatment. The uterine artery resistance index (RI),uterine artery pulsatility index (PI),and uterine artery peak systolic velocity (PSV) were measured by Doppler before and after treatment. The clinical efficacy and the occurrence of adverse reactions were compared between the two groups. ResultAfter treatment,the levels of MCP-1,TGF-β1,IL-6,ESR,and FIB decreased in both groups (P<0.01),and the decreases were larger in the observation group than in the control group (P<0.05,P<0.01). After treatment,the serum levels of CD4+ and CD4+/CD8+ elevated in both groups (P<0.01) and the observation group had higher levels of CD4+ and CD4+/CD8+ than the control group (P<0.05,P<0.01). The treatment in both groups decreased the TCM symptom score and TCM sign score and increased the SF-36 score (P<0.01),and the changes were more significant in the observation group than in the control group (P<0.05,P<0.01). In addition,the treatment lowered RI and PI and elevated PSV (P<0.01),and the changes in these indicators were more significant in the observation group than in the control group (P<0.01). The total response rate in the observation group was 93.67% (74/79),which was higher than that (79.75%,63/79) in the control group (χ2=6.645,P<0.05). There was no significant difference in the occurrence of adverse reactions between the two groups. ConclusionFor the patients with sequelae of pelvic inflammatory disease (syndrome of combined dampness,heat,and stasis),Qingre Huashi Sanjie enema prescription can reduce inflammation,attenuate hypercoagulability,improve hemodynamics,and regulate the immune function,demonstrating a definite therapeutic effect.
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@#Objective To investigate the neuroprotective effects of curcumin (CUR) on acute ischemic stroke (AIS) mice and to determine its effects on monocyte chemoattractant protein-1 (MCP-1) and C-C chemokine receptor 2 (CCR2) expression levels. Methods A permanent,focal cerebral infarction (dMCAO) model was established by cautery. Male C57BL/6 mice were randomly divided into a sham-operated (Sham),control (dMCAO),and CUR group. In the Sham group,only the common carotid artery was isolated and the middle cerebral artery branches were not cauterized. The CUR group was intraperitoneally administered CUR (200 mg/kg·d) for 7 consecutive days after dMCAO,and the dMCAO group was intraperitoneally administered an equal volume of solvent dimethyl sulfoxide. Cerebral infarct volume was calculated by the 2,3,5-triphenyltetrazolium chloride staining method,limb function was evaluated by the Rota-rod and Longa score. Western blot and immunofluorescence techniques were used to assess MCP-1 and CCR2 expression levels,and enzyme-linked immunosorbent assay (ELISA) was used to measure tumor necrosis factor (TNF)-α,interleukin (IL)-1β,and IL-6 expression levels. Results In the experiment,the dMCAO group showed higher modified Longa scores,shorter times on the roller,and larger infarct areas than the Sham group; the CUR group showed lower modified Longa scores,longer times on the Rota-rod,and smaller infarct areas than that of the dMCAO group. Western blot and immunofluorescence results showed that the expression of microglia,MCP-1,and CCR2 was significantly downregulated,and ELISA results showed that the expression levels of TNF-α,IL-1β,and IL-6 in mouse brain tissue were decreased. Conclusion CUR has a protective effect on AIS mice,and CUR can downregulate the expression of MCP-1 and CCR2 in mouse brain tissues,reduce the release of inflammatory factors,and exert its physiological functions.
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{L-End}Objective To analyze the changes of seven potential biomarkers in plasma of patients with occupational silicosis (hereinafter referred to as "silicosis"), and explore their clinical value in determining the stage of silicosis. {L-End}Methods A total of 100 male silicosis patients were selected as the silicosis group (63 cases in stage Ⅰ and 37 cases in stage Ⅱ subgroups), and 100 male healthy individuals were selected as the control group using the 1∶1 matched case-control study. Enzyme-linked immunosorbent assay was used to analyze the level of interleukin-17 (IL-17), monocyte chemoattractant protein-1 (MCP-1), matrix metalloproteinase-9 (MMP-9), Krebs von den Lungen-6 (KL-6), connective tissue growth factor (CTGF), platelet-derived growth factor (PDGF), and histone H4 in plasma. Their clinical value for diagnosing silicosis was evaluated using receiver operating characteristic (ROC) curve, discriminant analysis stepwise method, and Fisher discriminant function analysis. {L-End}Results The levels of IL-17, MCP-1, MMP-9, KL-6, CTGF, PDGF, and histone H4 in the plasma of the silicosis group, silicosis stage Ⅰ subgroups, and stage Ⅱ subgroups were higher than those in the control group (all P<0.05). The levels of IL-17, MCP-1, and MMP-9 in the plasma of the stage Ⅱ subgroup decreased (all P<0.05), while the levels of KL-6, CTGF and histone H4 increased (all P<0.05) compared with the stage Ⅰ subgroup. The area under the ROC curve for diagnosing silicosis using these seven potential biomarkers ranged from 0.761 to 1.000 (all P<0.01), with the sensitivity of 0.640-1.000, the specificity of 0.840-0.990, and the Youden index of 0.540-0.990. The Fisher discriminant function was formed by stepwise discriminant analysis, and the results showed that the coincidence rate was 99.5%, and the misdiagnosis rate was 0.5% for diagnosing and staging silicosis with these seven potential biomarkers. The coincidence rate of diagnosing control group, silicosis stageⅠsubgroup and the silicosis stage Ⅱ subgroup was 100.0%, 98.4% and 100.0%, respectively. {L-End}Conclusion IL-17, MCP-1, MMP-9, KL-6, CTGF, PDGF and histone H4 in plasma can be used as biomarkers for the diagnosis of silicosis, and the Fisher discriminant function based on the combination of these seven biomarkers can assist in staging silicosis.
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Objective:To explore the predictive values of serum monocyte chemoattractant protein-1 (MCP-1), high mobility protein B1 (HMGB1), adiponectin (APN) and oxidized low density lipoprotein (ox-LDL) levels on poor prognosis of patients with acute cerebral infarction(ACI).Methods:One hundred and sixty-fivepatients with ACI in Zibo Hospital, Shandong Guoxin Nursing Group from October 2018 to December 2020 were selected as the observation group, and 147 healthy people in the same period were selected as the normal control group. The levels of serum MCP-1, HMGB1, APN and ox-LDL were detected. In addition, the observation group was followed up for 3 months after discharge, and the observation group was divided into good prognosis group and poor prognosis group by modified Rankin Scale score. The levels of serum MCP-1, HMGB1, APN and ox-LDL between the poor prognosis group and the good prognosis group were compared. The influencing factors of poor prognosis in patients with ACI and the predictive value of serum MCP-1, HMGB1, APN and ox-LDL levels on poor prognosis were analyzed by Logistic multiple regression analysis and receiver operating characteristic (ROC) curve.Results:The levels of serum MCP-1, HMGB1 and ox-LDL in the observation group were higher than those in the normal control group: (322.61 ± 65.27) ng/L vs. (163.18 ± 15.12) ng/L, (6.61 ± 3.54) μg/L vs. (2.90 ± 0.41) μg/L, (481.11 ± 177.67) mg/L vs. (247.47 ± 27.13) mg/L; but the level of serum APN was lower than that in the normal control group: (10.63 ± 3.80) μg/L vs. (17.65 ± 2.87) μg/L, there were statistical differences ( P<0.05). After 3 months of follow-up, the incidence rate of poor prognosis in the observation group was 35.15%(58/165). The serum levels of MCP-1, HMGB1 and ox-LDL in the poor prognosis group were higher than those in the good prognosis group: (372.15 ± 71.33) ng/L vs. (295.76 ± 42.23) ng/L, (9.74 ± 3.96) μg/L vs. (4.91 ± 1.62) μg/L, (631.03 ± 196.84) mg/L vs. (399.85 ± 95.07) mg/L; but the serum APN level was lower than that in the good prognosis group: (7.62 ± 2.83) μg/L vs. (12.27 ± 3.22) μg/L, there were statistical differences ( P<0.05). The results of Logistic multiple regression analysis showed that age, hypertension, hyperlipidemia, infarct volume, nerve function defect score, time from onset to treatment and MCP-1, HMGB1, APN and ox-LDL levels were the influencing factors of poor prognosis in patients with ACI ( P<0.05). The results of ROC curve analysis showed that the sensitivity and area under the curve of serum MCP-1, HMGB1, APN and ox-LDL levels in combined predicting the poor prognosis were 98.28% and 0.954, which were higher than the single index evaluation ( P<0.05). Conclusions:The serum levels of MCP-1, HMGB1 and ox-LDL are closely related to the prognosis of ACI patients, and all of them have a certain predictive value for the poor prognosis of patients, but the combined prediction efficiency of four items is more higher.
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Objective:To explore the diagnostic accuracy of muscle ultrasound and plasma monocyte chemoattractant protein-1 (MCP-1) for ICU-acquired weakness (ICU-AW) in patients with sepsis.Methods:A prospective observational study was conducted. Patients with sepsis admitted to the intensive care unit (ICU) of Henan Provincial People's Hospital from April 2021 to October 2021 were enrolled. The demographic data were collected. The enrolled patients were evaluated with Medical Research Council (MRC) score every day until discharged from ICU. During this period, patients with total MRC score < 48 (for two consecutive times and a time interval of 24 hours) were divided into ICU-AW group, those with total MRC score ≥ 48 were served as non-ICU-AW group. On the 1st, 4th and 7th day following admission into ICU, ultrasound was used to measure the muscle linear thickness of the rectus femoris (RF-MLT), the cross sectional area of the rectus femoris (RF-CSA) and the muscle linear thickness of the vastus intermedius muscle (VI-MLT). And meanwhile, the plasmas samples of patients were collected to measure MCP-1 concentration by enzyme-linked immunosorbent assay (ELISA). The difference of each index was compared between the ICU-AW group and the non-ICU-AW group. The risk factors of ICU-AW in patients with sepsis were analyzed by binary Logistic regression. Besides, receiver operator characteristic curve (ROC curve) was plotted, the diagnostic value of ultrasound parameters and plasma MCP-1 level for ICU-AW in patients with sepsis was analyzed.Results:A total of 99 septic patients were enrolled, with 68 patients in the ICU-AW group and 31 patients in the non-ICU-AW group. Compared with the patients in the ICU-AW group, the patients in the non-ICU-AW group tended to be older, and had higher sequential organ failure assessment (SOFA) score, higher acute physiology and chronic health evaluation Ⅱ (APACHEⅡ) score, higher rates of septic shock, higher blood lactic acid and lower Glasgow coma score (GCS). Binary Logistic regression analysis showed that APACHEⅡ score and septic shock were the risk factors of ICU-AW for septic patients [odds ratio ( OR) and 95% confidence interval (95% CI) were 1.310 (1.138-1.509) and 0.232 (0.072-0.746), respectively, both P < 0.05]. The RF-MLT, RF-CSA and VI-MLT on the 1st, 4th and 7th ICU day was falling over time. Compared with the patients in the ICU-AW group, the patients in the non-ICU-AW group had smaller RF-MLT on the 7th day [cm: 0.32 (0.22, 0.47) vs. 0.45 (0.34, 0.63), P < 0.05] and higher 7-day RF-CSA atrophy rate [25.85% (10.37%, 34.28%) vs. 11.65% (2.28%, 22.41%), P < 0.05]. According to ROC curve analysis, 7-day RF-MLT had diagnostic value for ICU-AW of septic patients. Area under ROC curve (AUC) was 0.688 (95% CI was 0.526-0.849); when the cut-off value was 0.41 cm, the sensitivity and the specificity were 66.7% and 68.4%. The levels of plasma MCP-1 in the ICU-AW group were significantly higher than those in the non-ICU-AW group on the 1st, 4th and 7th day. ROC curve analysis showed that the plasma MCP-1 levels on the 1st, 4th and 7th day played a significant role to diagnose ICU-AW for septic patients, the AUC and 95% CI were 0.732 (0.629-0.836), 0.865 (0.777-0.953), 0.891 (0.795-0.986), respectively. When the cut-off values were 206.3, 410.9, 239.5 ng/L, the sensitivity was 87.1%, 64.0%, 82.4%, and the specificity was 54.4%, 96.1%, 86.2%, respectively. Conclusion:The muscle mass parameters on the 7th day of bedside ultrasound and plasma MCP-1 levels had certain diagnostic values for ICU-AW in patients with sepsis.
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Objective:To evaluate the role of monocyte chemoattractant protein-induced protein-1 (MCPIP-1) in acute lung injury in septic rats.Methods:Forty-eight healthy male Sprague-Dawley rats, aged 8-12 weeks, weighing 230-270 g, were divided into 6 groups ( n=8 each) using the random number table method: sham operation group (S group), different doses of ubiquitin-proteasome inhibitor groups (M 1 and M 2 groups), cecal ligation and perforation (CLP) group, and different doses of ubiquitin-proteasome inhibitor + CLP groups (M 1-CLP and M 2-CLP group). Sepsis was induced by CLP in anesthetized animals.Ubiquitin-proteasome inhibitor MG-132 5 and 10 mg/kg were intraperitoneally injected at 30 min before sham operation in M 1 and M 2 groups, respectively.MG-132 5 and 10 mg/kg were intraperitoneally injected at 30 min before CLP in M 1-CLP and M 2-CLP groups, respectively.The rats were sacrificed at 6 h after operation, bronchoalveolar lavage (BALF) was collected for determination of the concentrations of tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β) and IL-6 in BALF (by enzyme-linked immunosorbent assay) and lung tissues were obtained for microscopic examination of pathological changes which were scored and for determination of wet/dry lung weight ratio (W/D ratio) and expression of MCPIP-1 protein and mRNA (by Western blot and real-time polymerase chain reaction). Results:Compared with S group, the lung injury scores, W/D ratio, and concentrations of TNF-α, IL-1β and IL-6 in BALF were significantly increased in CLP group ( P<0.05), and no significant changes were found in the parameters mentioned above( P>0.05), and the expression of MCPIP-1 protein and mRNA in lung tissues was significantly up-regulated in M 1 and M 2 groups ( P<0.05), and no significant change was found in the expression of MCPIP-1 protein and mRNA in lung tissues in CLP group ( P>0.05). Compared with CLP group, the lung injury scores, W/D ratio, and concentrations of TNF-α, IL-1β and IL-6 in BALF were significantly decreased, and the expression of MCPIP-1 protein and mRNA in lung tissues was up-regulated in M 1-CLP and M 2-CLP groups ( P<0.05). Conclusions:MCPIP-1 exerts an endogenous protective mechanism during acute lung injury in septic rats.
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Objective To study the protective effect of quercetin on the kidney of mice with systemic lupus erythematosus (SLE) and to explore its effect on transforming growth factor (TGF)-β1 and monocyte chemoattractant protein-1 (MCP-1).Methods Thirty BALB/c female mice were randomly divided into control group,model group and drug group according to the envelope method,with 10 mice in each group.A mouse model of SLE was established by intra-peritoneal injection of pristane method.The drug group was given quercetin treatment,and the control group and the model group were given the same dose of normal saline.The renal function index and autoanti-body level in each group of mice were compared.The pathological changes of renal tissues were observed by HE staining.The expressions of TGF-β1 and MCP-1 were determined by Western blotting and real-time fluorescence quantitative reverse transcription polymerase chain reaction (qRT-PCR).The renal function index,autoantibody level,TGF-β1,and MCP-1 expression were statistically analyzed by analysis of one-way analysis of variance (ANOVA).Results The levels of blood urea nitrogen (BUN),serum creatinine (Scr),24 h urine protein,kidney hypertrophy index,antinuclear antibody (ANA) antibody,anti-dsDNA antibody and anti-snRNP/Sm in the model group and the drug group were higher than those in the control group.Compared with the model group,the levels of BUN,Scr,24 h urine protein,kidney hypertrophy index,ANA antibody,anti-dsDNA antibody,anti-snRNP/Sm in the drug group were(11.3±1.1) mmol/L,(45±4) μmol/L,(25.7±2.6) mg/24 h,(4.3±0.4)×10-3,(30.3±3.1) ng/L,(472±48) μmol/L and (17.6±1.8) ng/L,which were decreased (q =10.678,6.698,14.948,14.412,9.226,4.691,8.226,P<0.01).The glomerular score,tubulointerstitial score and tubulointer-stitial score of the model group were higher than those of the control group.The glomerular score,tubulointer-stitial score and tubular score of the drug group were lower than those of the model group (q=10.935,49.537,20.439,P<0.01).HE staining showed that the kidney structure of the control group was no obvious damage.In the model group,the glomerular volume of the mice increased,and the inflammatory cells in the renal interstitial and renal tubules infiltrated.The pathological changes in the drug group were significantly reduced compared with the model group.Compared with the control group,the expression levels of TGF-β1,MCP-1 protein and mRNA in the model group and the drug group were significantly increased.Compared with the model group,TGF-β1 and MCP-1 protein and mRNA expression levels the mice in the drug group were significantly reduced.Conclusion Quercetin can improve renal function in mice with SLE by down-regulating the expression of TGF-beta 1 and MCP-1.
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Objective@# To explore the role of lipopolysaccharide(LPS)in the pathogenesis of calcific aortic valve disease(CAVD)by detecting the expression of inflammatory factors in aortic valve interstitial cells(AVICs),and the expression of interleukin-6(IL-6),interleukin-8(IL-8),monocyte chemoattractant protein-1(MCP-1)after silencing pentraxin 3(PTX3)gene,to test the effect of PTX3 on the pathophysiological process of CAVD. @*Methods@#We obtained aortic valves for immunohistochemistry staining from 12 patients with CAVD,and from 12 patients without aortic valve disease receiving heart transplant operation as controlAVICs were cultured in vitro,different concentrations of LPS(0,50,100,200 ng/mL)treated cells for 24 h,and then the expression levels of IL-6,IL-8 and MCP-1 were analyzed by real-time polymerase chain reaction(real-time PCR). After AVICs were transfected with PTX3 siRNA for 48 h to knockdown the expression of PTX3 protein,PTX3 was tested by Western blotting. The levels of IL-6,IL-8 and MCP-1 were detected by real-time PCR 24 h after treatment with LPS(100 ng/mL)in AVICs with PTX3 siRNA transfection. @*Results@#The calcific aortic valves significantly expressed PTX3 as compared with control.LPS dose-dependently increased IL-6,IL-8 and MCP-1 in AVICs. Compared with control groups,100 ng/mL LPS significantly increased IL-6,IL-8 and MCP-1 mRNA(P<0.05,P<0.01). PTX3 siRNA markedly decreased the levels of PTX3 protein compared with control groups(P<0.01). Levels of IL-6,IL-8 and MCP-1 were significantly reduced in LPS plus PTX3 siRNA group compared with controls(all P<0.05).@*Conclusion@#The calcific aortic valves have a higher level of PTX3 than control valves.LPS stimulates the expression of IL-6,IL-8 and MCP-1 in AVICs,but silencing PTX3 gene significantly inhibits LPS-stimulated expression of IL-6,IL-8 and MCP-1. PTX3 may play a role in CAVD pathogenesis by regulating expression of inflammatory factors
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@#AIM: To observe the effect of pigment epithelium-derived factor(PEDF)on retinal neovascularization(RNV)and monocyte chemoattractant protein-1(MCP-1)expressions in mice retina of oxygen-induced retinopathy(OIR), and to investigate the protective effect of PEDF on ischemia hypoxia retinopathy and the possible mechanism. <p>METHODS: A total of 160 postnatal day(P)7 C57BL/6 mice were obtained. All mice except normal control group were exposed to(75±2)% oxygen environment for 5d and then kept in room air for another 5d to establish the OIR mice model. All mice in normal control group(40 mice)were exposed to room air only. At P12 and P14, respectively, mice in PEDF treatment group were injected intravitreously with recombinant human PEDF(2μg/eye,1μL)in the right eye, while mice in treatment control group were injected intravitreously with the same volume of vehicle [1μL, 10mmol/L phosphate buffered saline(PH7.4), PBS] in the right eye. All mice were euthanized at P17. Eyes were whole mounted and stained with Lectin to observe the growth of abnormal RNV; And retinal specimens were prepared for PEDF, MCP-1 protein and mRNA analysis by Western blot and real time RT-PCR respectively. <p>RESULTS: Changes of retinal vessels had been detected by fluorescence microscopy on flat-mounted retina. The relative RNV areas were significantly increased in OIR model group compared with those in normal control group(<i>P</i><0.01). However, the relative RNV areas were significantly reduced in PEDF treatment group compared with those in PBS treatment control group(<i>P</i><0.01). The specific expression of MCP-1 protein and mRNA in the OIR model group were higher than those of normal control group, presenting a statistically significance(both <i>P</i><0.05). The specific expression of PEDF protein and mRNA in the OIR model group showed a considerable decline in comparison with normal control group, presenting a statistically significance(both <i>P</i><0.01). And the specific expression of MCP-1 protein and mRNA in those of PEDF-treated group showed a considerable decline in comparison with PBS-treated group, and the differences were statistically significant(both <i>P</i><0.05). However, there were increase of the expression of MCP-1 protein and mRNA between normal control group and PEDF-treated group, presenting no statistically significance(both <i>P</i>>0.05). <p>CONCLUSION: PEDF could inhibit oxygen-induced retinal neovascularization and down-regulate retinal MCP-1 expression under hypoxia, which may underlie its anti-neovascularization effects and play a role of protection in ischemic retinopathy.
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Objective To explore the dynamic changes of serum monocyte chemoattractant protein-1 (MCP-1) and interleukin-6 (IL-6) in patients with acute pancreatitis (AP) and its clinical significance.Methods A total of 103patients with AP admitted to our hospital from June 2016to December 2017were selected, which were divided into mild AP (MAP group, n=62) and severe AP (SAP group, n=41) according to the condition of disease.The levels of serum MCP-1and IL-6at 1st, 3rd, 7th day after admission were determined by the radioimmunoassay.At the same time, a total of 40healthy volunteers as control group were randomly selected.The predictive value of serum MCP-1and IL-6on for AP was analyzed.Results The serum MCP-1, IL-6level and APACHEⅡscore of MAP group and SAP group at 1st day were higher than those of control group (P<0.05) .The serum MCP-1, IL-6level and APACHEⅡscore of MAP group and SAP group at 3rd, 7th day were higher than those at 1st, and which at 7th were lower than those at 3rd (P<0.05) .The serum MCP-1, IL-6level and APACHEⅡscore of SAP group at 1st, 3rd, 7th were higher than those of MAP group (P<0.05) .Among patients with AP, serum MCP-1and IL-6were positively associated with APACHEⅡscore (P<0.05) .The best cutoff value of serum MCP-1for AP was 31.6pg/mL, and the area under ROC curve was 0.852, and the sensitivity and specificity was 0.87and 0.82respectively, and the accuracy was 0.85.The best cutoff value of serum IL-6for AP was 35.9ng/L, and the area under ROC curve was 0.876, and the sensitivity and specificity were 0.91and 0.85respectively, and the accuracy was 0.87.Conclusion The serum MCP-1and IL-6of patients with AP abnormal changes, which were closely related to the severity and prognosis.Early detection of MCP-1and IL-6can help to judge condition and evaluate prognosis.
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Objective To measure the levels of monocyte chemoattractant protein-1 (MCP-1) in the aqueous humor of patients with acute primary angle-closure glaucoma (APACG),and its correlation with the patients' prognosis after trabeculectomy.Methods This retrospective case-control study included 19 patients with APACG who experienced a failed trabeculectomy (case group) and 57 age-and sex-matched patients with APAGG who underwent successful trabeculectomy (control group).Aqueous humor was collected before trabeculectomy for the detection of MCP-1 levels in the both groups by enzyme-linked immunosorbent assay.And finally,logistic regression analysis was applied to assess the risk factors for failed trabeculectomy.Results The MCP-1 concentration in aqueous humor was (5688.04 ± 2099.99)ng · L-1 in the case group and (2077.57 ± 568.44)ng · L-1 in the control group,and the difference between both groups were significant (P < 0.001).Logistic regression analysis revealed MCP-1 level (OR =1.005;95% CI =1.001-1.008) and a shallow anterior chamber after surgery (OR =31.430;95% CI =1.577-57.350) were the independent risk factors for failed trabeculectomy procedures.Conclusion MCP-1 levels in aqueous humor are higher in APACG eyes with failed trabeculectomy than those with successful one during 1-year follow-up,so MCP-1 level is considered as an independent risk factor for failed trabeculectomy.
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AIM:To investigate the possible mechanism of resveratrol(Res)on tumor necrosis factor-α (TNF-α)-induced monocyte chemoattractant protein-1(MCP-1)expression in primary rat pulmonary artery endothelial cells(RPAECs).METHODS: RPAECs were randomly divided into 4 groups: control group, solvent(1% DMSO) group,TNF-αgroup and Res group.Each group was divided into 1 h,4 h and 8 h subgroups(n=6 per time point).The TNF-α+C1142(a rodent chimeric mAb that neutralizes rat MCP-1)group was set up at the 8 h time point.At each time point,the protein and mRNA expression of MCP-1 was measured by Western blot and real-time PCR.RESULTS: Pre-treatment of the RPAECs with C1142 significantly down-regulated the expression of MCP-1(P<0.05).The protein and mRNA expression of MCP-1 was markedly increased in TNF-αgroup(P<0.05).Notably,incubation with Res down-re-gulated the protein and mRNA expression of MCP-1,which was significantly lower than that in TNF-αgroup(P<0.05). CONCLUSION:MCP-1 was involved in the process of TNF-α-induced injury of RPAECs.Res down-regulates the expres-sion of MCP-1 in RPAECs,thus attenuating cell injury.
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Mounting evidence supports an important role of chemokines, produced by spinal cord astrocytes, in promoting central sensitization and chronic pain. In particular, CCL2 (C-C motif chemokine ligand 2) has been shown to enhance N-methyl-D-aspartate (NMDA)-induced currents in spinal outer lamina II (IIo) neurons. However, the exact molecular, synaptic, and cellular mechanisms by which CCL2 modulates central sensitization are still unclear. We found that spinal injection of the CCR2 antagonist RS504393 attenuated CCL2- and inflammation-induced hyperalgesia. Single-cell RT-PCR revealed CCR2 expression in excitatory vesicular glutamate transporter subtype 2-positive (VGLUT2) neurons. CCL2 increased NMDA-induced currents in CCR2/VGLUT2 neurons in lamina IIo; it also enhanced the synaptic NMDA currents evoked by dorsal root stimulation; and furthermore, it increased the total and synaptic NMDA currents in somatostatin-expressing excitatory neurons. Finally, intrathecal RS504393 reversed the long-term potentiation evoked in the spinal cord by C-fiber stimulation. Our findings suggest that CCL2 directly modulates synaptic plasticity in CCR2-expressing excitatory neurons in spinal lamina IIo, and this underlies the generation of central sensitization in pathological pain.
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Animals , Female , Male , Mice , Benzoxazines , Pharmacology , Therapeutic Uses , Chemokine CCL2 , Genetics , Metabolism , Pharmacology , Excitatory Amino Acid Agents , Pharmacology , Excitatory Amino Acid Agonists , Pharmacology , Freund's Adjuvant , Toxicity , Hyperalgesia , Metabolism , Long-Term Potentiation , Physiology , Luminescent Proteins , Genetics , Metabolism , Mice, Inbred C57BL , Mice, Transgenic , Myelitis , Drug Therapy , Metabolism , Neurons , Pain Management , Somatostatin , Genetics , Metabolism , Spinal Cord , Cell Biology , Spiro Compounds , Pharmacology , Therapeutic Uses , Vesicular Glutamate Transport Protein 2 , Genetics , Metabolism , Vesicular Inhibitory Amino Acid Transport Proteins , Genetics , MetabolismABSTRACT
Objective To explore the correlation between chemokine C-C motif ligand 2 (CCL2)-2518A/G polymorphism and the incidence of systemic lupus erythematosus (SLE),and investigate the effects of CCL2-2518A/G polymorphism on the expression of CCL2.Methods A total of 134 SLE patients and 56 sex and age matched healthy people were enrolled in this study.CCL2 plasma levels were measured by enzymelinked immunosorbent assay(ELISA).The 2518 A/G polymorphism in CCL2 promoter region was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP),and then peripheral blood mononuclear cells (PBMCs) were cultured in vitro to explore the influence of the 2518A/G polymorphism in CCL2 promoter region on the expression of CCL2.Mann-Whitney U-test,Student's t test and chi-squared test were used for analysis.Results The plasma CCL2 level in the SLE group was 358.5 (500.1) pg/ml [median (four interval)],which was significantly higher than that in the control group 243.6(125.8) pg/ml (Z=3.892,P=0.000).Patients with high plasma CCL2 levels were more prone to have renal (x2=7.159,P=0.007) and der-matomucosal (x2=5.133,P=0.023) involvement,as well as much higher disease activity index (SLEDAI) scores (Z=2.012,P=0.047).The results of the analysis of individual CCL2-2518A/G polymorphic genotypes suggested that patients with the G/G genotype had the highest CCL2 levels 425.7 (608.8) pg/ml,followed by those with the G/A genotype 355.3(511.1) pg/ml and A/A genotype 327.8(367.9) pg/ml (x2=3.496,P=0.048).The results of in vitro experiment showed that after the stimulation of lipopolysaccharide,the expression of CCL2 in PBMCs with G/G homozygote increased more significantly than that with A/A homozygote (P<0.05).Conclusion The increase of plasma CCL2 concentrations is associated with tissue injury and high SLEDAI,which suggests that CCL2 may play a crucial role in the pathogenesis of SLE.CCL2-2518A/G polymorphism is not related to the pathogenesis of SLE,but it can affect the condition of SLE by promoting the expression of CCL2 in inflammatory environment.
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OBJECTIVE@#To study the effects of astragaloside-IV (As-IV) on the expression of inflammatory factor and proliferation of glomerular mesangial cells (GMCs) induced by angiotensin Ⅱ(AngⅡ).@*METHODS@#The model of diabetic nephropathy(DN) was mimic by angiotensin Ⅱ (10mol/L)inducing GMCs injury. Then the GMCs were treated with As-IV at different concentrations(25,50,100 μmol/L)for 48 hours. The proliferation of GMCs was detected by MTT. The level of reactive oxidative species (ROS) was measured by flow cytometry. The expression of monocyte chemoattractant protein-1(MCP-1) protein in supernatant was detected by enzyme- linked immunosorbent assay (ELISA). The expression of transforming growth factor-β1(TGF-β1) in GMCs was measured by Western blot.@*RESULTS@#Compared with model group, the proliferation of GMCs was inhibited in As-IV group. As-IV decreased the level of intercellular ROS, down-regulated the secretion of MCP-1 and the expression of TGF-β1 proteins.@*CONCLUSIONS@#As-IV could inhibit cell proliferation and inflammatory factors expression on GMCs induced by AngⅡ.
Subject(s)
Humans , Angiotensin II , Blotting, Western , Cell Proliferation , Cells, Cultured , Diabetic Nephropathies , Mesangial Cells , Transforming Growth Factor beta1ABSTRACT
Objective To investigate the effects of bone marrow mesenchymal stem cells (BMSC) on the expression of inflammatory factors in rats with multiple organ dysfunction syndrome (MODS). Methods BMSC extracted from the 4-week-old Sprague-Dawley (SD) rats was cultivated and identified in vitro, then the 4th passage of which was used in the experimental study. Sixty SD rats were randomly(random number) divided into three groups (n=20 in each group): Sham group (SG), MODS group (MG) and BMSC group (BG). Rats in the MG was injected by 1 mg/kg lipopolysaccaride (LPS) via great saphenous vein, rats in the SG injected with the same volume sterile phosphate buffer saline and rats in the BG infused by 1×106/cells BMSCs through the tail vein at 2 h after LPS injection. The survival rate, tissue pathological changes of the lung, liver and heart by hematoxylin and eosin (HE) staining, organ dysfunction measurement by blood gas analysis and biochemical indicators as well as the related inflammatory factors by protein microarray and enzyme linked immunosorbent assay (ELISA), were detected 72 h post operation. Multi-group quantitative data was analyzed by one way ANOVA, paired-comparisons by LSD-t test and the comparisons of survival curves in the three groups by Log-rank test. The value of P<0.05 was considered statistically significant. Results The survival rate in SG, MG and BG was 100%, 60% and 80%, respectively. The survival curves showed that the survival rate of SG was higher than the MG and BG (SG vs. MG, χ2=9.798, P=0.0017; SG vs. BG, χ2=4.333, P=0.0374), but there was no significant difference comparing the BG to the MG (χ2=2.408, P=0.1207). The tissue congestion and edema, and inflammatory cells infiltration in the lung, liver, and heart of the MG were observed by HE staining, while these changes reduced in the BG. Compared with the SG, the levels of pH and PaCO2 and lactic acid (Lac) increased significantly (all P<0.01), the level of total bilirubin (TB) significantly increased [(0.801±0.501)U/L vs. (2.533±0.382)U/L, P=0.003], while the albumin(ALB) level decreased significantly[(35.471±4.015)U/L vs. (23.202±4.872)U/L, P<0.01], and creatine kinase (CK) level increased significantly in MG [(315.670±41.402) vs. (708.250±219.201), P=0.042]. After BMSC treatment, the organ function improved significantly (all P<0.05). Gamma interferon (IFN-γ) and monocyte chemotactic protein 1 (MCP-1) were the differential expression factors in protein chips. The results of ELISA were similar to the protein chips: compared with the SG, IFN-γ and MCP-1 expressions in the MG increased significantly (P<0.01). Compared with MG, the expressions of IFN-γ and MCP-1 decreased significantly in the BG (P<0.01). Conclusion BMSC administration could modulate the inflammatory response of MODS rats by inhibiting the levels of IFN-γ and MCP-1, and improve the organ function and the survival rate.
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OBJECTIVES: Henoch-Schönlein purpura nephritis and immunoglobulin A nephropathy are two diseases with similar clinical presentations but very different prognoses. Transforming growth factor β1 and monocyte chemoattractant protein-1 have been associated with the development of tissue fibrosis. We examined the development of tubulointerstitial fibrosis and its relationship with Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in these patients. METHODS: Renal tissue samples were collected by renal biopsy from 50 children with Henoch-Schönlein purpura nephritis and 50 children with immunoglobulin A nephropathy. Hematoxylin and eosin and Masson's trichrome-stained tissues were examined using light microscopy. Tubulointerstitial fibrosis was graded using the method described by Bohle et al. (1). The immunohistochemical detection of Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was correlated with the tubulointerstitial fibrosis grade. Clinical Trial registration number: ZJCH-2012-0105. RESULTS: Transforming growth factor β1 and monocyte chemoattractant protein-1 expression in the renal tissues was significantly greater in the patients with immunoglobulin A nephropathy than in the patients with Henoch-Schönlein purpura nephritis (both p<0.001). The immunoglobulin A nephropathy patients had a higher tubulointerstitial fibrosis grade than the Henoch-Schönlein purpura nephritis patients (p<0.001). The tubulointerstitial fibrosis grade was in accordance with the Transforming growth factor β1 and monocyte chemoattractant protein-1 expression levels in both diseases (both p<0.001). CONCLUSION: Transforming growth factor β1 and monocyte chemoattractant protein-1 expression was associated with the development of immunoglobulin A nephropathy and Henoch-Schönlein purpura nephritis. Further studies are needed to better evaluate this association.
Subject(s)
Humans , Male , Female , Child, Preschool , Child , Adolescent , IgA Vasculitis/metabolism , Chemokine CCL2/metabolism , Transforming Growth Factor beta1/metabolism , Glomerulonephritis, IGA/metabolism , Kidney Tubules/metabolism , Prognosis , IgA Vasculitis/pathology , Fibrosis , Glomerulonephritis, IGA/pathology , Kidney Tubules/pathologyABSTRACT
Objective To investigate the effect of Vitamin D (VitD) on intraperitoneal fat coefficient,monocyte/macrophage chemoattractant protein and macrophage infiltration in adipose tissue of infantile rats with obesity.Methods A total of 45 weanling female SD rats were randomly divided into control group (group N),obesity model group(group OB) and VitD intervention group(group VitD),and each group had 15 rats.The rats of group N were fed with basic diet,and the rats in group OB and group VitD were fed with high-fat diet.The rats of group VitD were administrated intragastrically with VitD 5 μg/(kg · d)(equivalent to 400 IU VitD for human infants) for 6 weeks,while the rats of group OB and group N were given plant oil [5 mL/(kg · d)] for 6 weeks instead.The body weight of rats were recorded once every week,and Lee's indexes were calculated.The fat mass in enterocoelia were wcighted after 6 weeks.The levels of monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein-1 α (MIP-1 α) in serum were detected by adopting enzyme-linked immunosorbent assay.The specimens of adipose tissue were observed and the number of adipocyte was counted through hematoxylin-eosin stain.The protein expressions of MCP-1,MIP-1 α and F4/80 in adipose tissue were determined by immunohistochemistry,and the mRNA expressions of MCP-1,MIP-1α and nuclear factor (NF)-κB in adipose tissue were determined by real time quantitative polymerase chain reaction(qPCR),then the correlation analysis with body weight,Lee's index and fat mass in enterocoelia were conducted.Results After 6 weeks with high-fat diet,the body weight,intraperitoneal fat coefficient,serum levels ofMCP-1 and MIP-1α in group OB[(244.1 ± 16.2) g,(3.25 ±0.63)%,(2 275.2 ±229.3) ng/L,(190.4 ± 61.9) ng/L] significantly increased compared with those of group N [(224.2 ± 10.9) g,(2.43 ± 0.47) %,(1 522.1 ±577.1) ng/L,(63.6 ±31.6) ng/L] and group VitD[(214.0± 12.5) g,(2.04 ±0.64)%,(1 863.4 ± 477.0) ng/L,(120.3 ± 29.5) ng/L],and the differences were significant (all P < 0.05).The adipose cells ranged orderly in group N and group VitD;the structure was disordered in group OB with various shapes and sizes of adipose cells and the excessively expanded adipose cells existed with many small newborn adipose cells.Immunohistochemistry showed that the protein expressions of MCP-1,MIP-1α and F4/80 in adipose tissue in group OB(130 944.5 ±10 706.1,174 354.8 ±65 267.8,51 701.9 ± 50 105.1) significantly increased compared with those of group N (47 394.5 ± 9 261.9,54 376.7 ± 36 436.9,23 370.3 ± 16 613.1),and the differences were significant (all P < 0.01);the protein expressions of MCP-1,MIP-1α and F4/80 in adipose tissue in group VitD (102 967.2 ± 9 329.3,48 659.8 ± 43 553.8,25 604.9 ± 11 411.6) significantly decreased compared with those of group OB,and the differences were significant (all P < 0.01).The qPCR showed that mRNA expressions of MCP-1,MIP-1 α and NF-κB in adipose tissue in group OB (2.78 ± O.90,7.10 ± 1.85,1.50 ± 0.16) significantly increased compared with those of group N (0.88 ± 0.18,0.99 ± 0.80,1.00 ± 0.28),and the differences were significant (all P < 0.05);the mRNA expressions of MCP-1,MIP-1α and NF-κB in adipose tissue in group VitD(1.73 ±0.51,1.59 ± 1.09,0.72 ±0.30) significantly decreased compared with those of group OB,and the differences were significant (all P <0.05).There was no significant difference in Lee's indexes among the 3 groups (F =0.351,P =0.711).At the age of 9 months age,the mRNA expression levels of MCP-1,MIP-1α and NF-κB in adipose tissue of infantile rats were positively correlated with body weight and intra-peritoneal fat coefficient(r =0.738,0.517,0.762,0.693,0.519,0.557,all P < 0.05),but there was no correlation with the Lee's index(r =0.322,0.317,-0.023,all P >0.05).Conclusions VitD supplement can suppress the obesity induced by high-fat-diet,and the possible mechanism is that VitD reduce the expression of monocyte/macrophage chemoattractant protein and macrophage infiltration in adipose tissue through regulating NF-κB signal pathway.
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Objective To investigate both in mechanism of hyperoxia-induced acute lung injury (HALI) by vivo experiment,to observe the Bruton' s tyrosine kinase (Btk) and nuclear factor kappa B (NF-κB) signals expression level.Methods Total of 72 healthy male Kunming mice were randomly (random number) divided into four groups:air control group,hyperoxia exposure 3 days group (H3d group),hyperoxia exposure 3 days + inhibitor group (H3d + Ⅰ group) and inhibitor groups.Then the pathological changes of lung tissues were observed under light microscope;The total protein content (TP) of bronchoalveolar lavage fluid (BALF) and wet/dry weight ratio (W/D) of lung were detected;The protein expression of Btk,p-Btk,pNF-κB p65 were mersured by Western blot;tlhe mRNA level of IL-6 was determined by real-time polymerase chain reaction (qRT-PCR);the level of monocyte chemoattractant protein-1 (MCP-1) in serum was detected by enzyme-linked immunosorbent assay (ELISA).Statistcal significance was determined by 1-way ANOVA.Results There were no significant difference in the data between the control group and the inhibitor group (P > 0.05).The pathological injury in light microscope,content of total protein in BALF,W/D ratio of lung tissues in H3d group were significantly higher than H3d + Ⅰ group (Respectively P =O.002,P =0.000).Western blot analysis showed that expression of Btk,p-Btk,pNF-κB p65 in H3d group were significantly higher than those in H3d + Ⅰ group (Respectively P =0.002,P =0.013,P =0.000).RT-qPCR results showed that the expression of IL-6 mRNA in H3d group were significantly higher than control group (P =0.004),inhibitor group (P =0.000) and H3d + Ⅰ group (P =0.021).In addition,The serum MCP-1 levels in H3d group were higher markely than the control group (P =0.002),inhibitor group (P =0.000) and H3d + Ⅰ group (P =0.009).The correlation analysis showed that pNF-κB p65 were positively correlated wiht Btk and p-Btk (r =0.902 and 0.954,P < 0.01).Conclusions Btk may trigger the release of IL-6 and MCP-1 by mediating the signaling pathway of NF-κB in vivo study,which was most important in the occurrence of HALI.Therefore,inhibiting the Btk activity would alleviate the severity of lung injury effectively.
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Objective:To investigate the relationship between CD 4+CD25+regulatory T cells ( Treg) and monocyte chemoat-tractant protein-1 and its mechanism in KD pathogenesis .Methods:48 patients of KD (28 cases of recovery ,20 cases of acute phase ) were admitted from June 2014 to June 2015 and the other 40 cases of healthy children was admitted to control group .The levels of serum interleukin-15,17,23 (IL-15,17,23) and MCP-1 of two groups were measured with ELISA.The levels of Treg/Th17 cell ratio of two groups were measured with flow cytometry .Results:The levels of IL-15,IL-17,IL-23 and MCP-1 of KD group were higher than control groups(P<0.05) and the levels of IL-15,IL-17,IL-23 and MCP-1 of acute phase groups were higher than recovery groups .The levels of Th17,Treg cells,Th17/Treg of KD group were lower than the control group (P<0.05),while the levels of Th17,Treg cells,Th17/Treg cells in the acute phase of KD patients were higher than stable phase .The levels of IL-15,IL-17,IL-23 and MCP-1 and Treg/Th17 were negative correlation with univariate analysis by Pearson (P<0.05).Conclusion:The imbalance between Treg and Th17 cells and MCP-1 levels continue to rise may be associated with KD onset and progress of the disease is closely related to children in KD vivo by meas -uring children with KD Treg/Th17 cells and MCP-1 ratio of assessment Children with the condition and prognosis has some signifi-cance.