目的观察单核细胞趋化蛋白-1(MCP-1)、转化生长因子β_(1)(TGF-β_(1))、肿瘤坏死因子(TNF-α)在不同分期糖尿病肾病(DN)患者表达水平的差异,分析其与DN严重程度的相关性。方法选取2019年3月至2020年5月河南省人民医院收治的103例2型糖...目的观察单核细胞趋化蛋白-1(MCP-1)、转化生长因子β_(1)(TGF-β_(1))、肿瘤坏死因子(TNF-α)在不同分期糖尿病肾病(DN)患者表达水平的差异,分析其与DN严重程度的相关性。方法选取2019年3月至2020年5月河南省人民医院收治的103例2型糖尿病(T2DM)患者,根据尿微量白蛋白排泄率(UAER)的差异将患者分为单纯T2DM组(24 h UAER<30 mg)35例、早期尿蛋白组(30 mg<24 h UAER<300 mg)36例,临床尿蛋白组(24 h UAER>300 mg)32例;选取同期在河南省人民医院进行体检的40例健康志愿者作为健康对照组。采集各组受检者血清样本,采用酶联免疫吸附法检测各组患者MCP-1、TGF-β_(1)、TNF-α水平;分析MCP-1、TGF-β_(1)、TNF-α水平与24 h UAEER的相关性。结果单纯T2DM组、早期尿蛋白组、临床尿蛋白组患者血清MCP-1、TGF-β_(1)、TNF-α水平高于健康对照组,差异有统计学意义(P<0.05);随着DN病情的不断加重,患者血清MCP-1、TGF-β_(1)、TNF-α水平随之升高。MCP-1、TGF-β_(1)、TNF-α在DN各阶段与UAER呈正相关(P<0.05)。结论MCP-1、TGF-β_(1)、TNF-α表达水平随着DN病情加重不断升高,检测MCP-1、TGF-β_(1)、TNF-α在患者血清中的表达水平可以作为判断DN疾病发展的重要指标。展开更多
目的分析感染性休克患者血清炎症因子水平变化。方法选择2013年3月—2015年3月医院治疗的50例感染性休克患者作为观察组(n=50),并根据患者组患者在入院后是否发生多器官功能衰竭来分为发生组(n=21)及未发生组(n=29)。同期选取体检的50...目的分析感染性休克患者血清炎症因子水平变化。方法选择2013年3月—2015年3月医院治疗的50例感染性休克患者作为观察组(n=50),并根据患者组患者在入院后是否发生多器官功能衰竭来分为发生组(n=21)及未发生组(n=29)。同期选取体检的50例健康人员作为对照组(n=50)。ELISA法检测血标本中血清趋化因子(CXCL-8)和单核细胞趋化蛋白1(MCP-1)的水平。结果发生组及未发生组患者血清CXCL-8及MCP-1水平明显高于对照组(CXCL-8, 6.02±0.54 vs. 1.02±0.22;4.33±0.38 vs. 1.02±0.22;MCP-1,201.33±28.13 vs. 20.62±10.62;170.12±30.31 vs. 20.62±10.62),对比差异均具有统计学意义(P <0.05);发生组患者血清CXCL-8及MCP-1水平明显高于未发生组(CXCL-8:6.02±0.54 vs. 4.33±0.38;MCP-1:201.33±28.13 vs. 170.12±30.31),两组间对比差异具有统计学意义(P <0.05)。结论感染性休克患者血清CXCL-8及MCP-1水平明显升高,且发生多器官功能衰竭的患者血清CXCL-8及MCP-1水平更高。临床上应密切关注感染性休克患者两种炎症因子变化,进而制定合理的治疗方案。展开更多
Objective To investigate expression differences of neutrophil and mononuclear phagocyte related gene mRNAs among acute myocardial infarction （AMI）, stable angina （SA） and control groups, and then discuss their exp...Objective To investigate expression differences of neutrophil and mononuclear phagocyte related gene mRNAs among acute myocardial infarction （AMI）, stable angina （SA） and control groups, and then discuss their expression characteristics in the stable angina pectoris （SAP） and AMI stages of coronary artery disease （CAD）. Methods Whole Human Genome Oligo Microarrays were applied to assess the differential expression characteristics of neutrophil and mononuclear phagocyte related mRNAs in patients with AMI （n = 20）, SA （n = 20） and controls （n = 20）. Results （1） Almost all colony-stimulating factors （CSF） and their receptors related mRNAs was up-regulated in AMI and SA groups compared with the control group, and the expression of granulocyte-macrophage colony stimulating factor receptor （GM-CSFR） and granulocyte colony stimulating factor receptor （G-CSFR） mRNAs in the AMI group was significantly up-regulated compared with the other two groups （P 〈 0.01）. （2） The expression of mRNAs related to monocyte chemoattractant protein-1 （MCP-1）, CCR2 （MCP-1 receptor） and CXCR2 （IL-8 receptor） was significantly up-regulated （P 〈 0.01） in AMI group compared with SA and control groups IL-8 mRNA expression in the AMI group was clearly higher than the controls （P 〈 0.05）. （3） All mRNAs expression related to opsonic re- ceptors （IgG FoR and C3bR/C4bR） was significantly up-regulated in AMI group compared with SA and control group （P 〈 0.01）, and the SA group showed an upward trend compared with controls. （4） Most pattern recognition receptor （PRR）-related mRNAs expression was up-regulated in AMI group compared with SA and control groups. Most toll-like receptor （TLR） mRNAs expression was significantly up-regulated （P 〈 0.01） than the SA and control groups, macrophage scavenger receptor （MSR） mRNA was significantly up-regulated in AMI group compared with the control group （P 〈 0.01）, and the SA group showed an upward trend compared with the controls. Conclusions The expression of most neutrophil and mononuclear-macrophage function related genes mRNAs was significantly up-regulated by stages during the progression of CAD, suggesting that the adhesive, chemotactic and phagocytic functions of neutrophil and mononudear-macrophage were strengthened in the occurrence and development of coronary atherosclerosis and AMI. This also showed a stepped up- ward trend as the disease progressed.展开更多
AIM:To investigate the effect of age on severity of acute pancreatitis(AP) using biochemical markers,histology and expression of the protective pancreatitisassociated proteins(PAPs).METHODS:AP was induced via intraduc...AIM:To investigate the effect of age on severity of acute pancreatitis(AP) using biochemical markers,histology and expression of the protective pancreatitisassociated proteins(PAPs).METHODS:AP was induced via intraductal injection of 4% sodium taurocholate in young and old rats.Sera and pancreata were assayed at 24 h for the parameters listed above;we also employed a novel molecular technique to assess bacterial infiltration using polymerase chain reaction to measure bacterial genomic ribosomal RNA.RESULTS:At 24 h after induction of AP,the pancreata of older animals had less edema(mean ± SE histologic score of young vs old:3.11 ± 0.16 vs 2.50 ±-0.11,P < 0.05),decreased local inflammatory response(histologic score of stromal infiltrate:3.11 ± 0.27 vs 2.00 ± 0.17,P < 0.05) and increased bacterial infiltration(174% ± 52% increase from sham vs 377% ± 4%,P < 0.05).A decreased expression of PAP1 and PAP2 was demonstrated by Western blotting analysis and immunohistochemical staining.There were no differences in serum amylase and lipase activity,or tissue myeloperoxidase or monocyte chemotactic protein-1 levels.However,in the most-aged group,serum C-reactive protein levels were higher(young vs old:0.249 ± 0.04 mg/dL vs 2.45 ± 0.68 mg/dL,P < 0.05).CONCLUSION:In older animals,there is depressed PAP expression related to a blunted inflammatory response in AP which is associated with worsened bacterial infiltration and higher C-reactive protein level;this may explain the more aggressive clinical course.展开更多
AIM:To investigate the effect of administration of agmatine(AGM) on gastric protection against ischemia reperfusion(I/R) injury.METHODS:Three groups of rats(6/group);sham,gastric I/R injury,and gastric I/R + AGM(100 m...AIM:To investigate the effect of administration of agmatine(AGM) on gastric protection against ischemia reperfusion(I/R) injury.METHODS:Three groups of rats(6/group);sham,gastric I/R injury,and gastric I/R + AGM(100 mg/kg,i.p.given 15 min prior to gastric ischemia) were recruited.Gastric injury was conducted by ligating celiac artery for 30 min and reperfusion for another 30 min.Gastric tissues were histologically studied and immunostained with angiopoietin 1(Ang-1) and Ang-2.Vascular endothelial growth factor(VEGF) and monocyte chemoattractant protein-1(MCP-1) were measured in gastric tissue homogenate.To assess whether AKt/phosphatidyl inositol-3-kinase(PI3K) mediated the effect of AGM,an additional group was pretreated with Wortmannin(WM)(inhibitor of Akt/PI3K,15 μg/kg,i.p.),prior to ischemic injury and AGM treatment,and examined histologically and immunostained.Another set of experiments was run to study vascular permeability of the stomach using Evan's blue dye.RESULTS:AGM markedly reduced Evan's blue dye extravasation(3.58 ± 0.975 μg/stomach vs 1.175 ± 0.374 μg/stomach,P < 0.05),VEGF(36.87 ± 2.71 pg/100 mg protein vs 48.4 ± 6.53 pg/100 mg protein,P < 0.05) and MCP-1 tissue level(29.5 ± 7 pg/100 mg protein vs 41.17 ± 10.4 pg/100 mg protein,P < 0.01).It preserved gastric histology and reduced congestion.Ang-1 and Ang-2 immunostaining were reduced in stomach sections of AGM-treated animals.The administration of WM abolished the protective effects of AGM and extensive hemorrhage and ulcerations were seen.CONCLUSION:AGM protects the stomach against I/R injury by reducing vascular permeability and inflammation.This protection is possibly mediated by Akt/PI3K.展开更多
Objective To investigate the effects of stimulant for nucleotide-binding oligomerization domain 1 （NOD1） on secretion of proinflammatory chemokine/cytokines and insulin-dependent glucose uptake in human differentiat...Objective To investigate the effects of stimulant for nucleotide-binding oligomerization domain 1 （NOD1） on secretion of proinflammatory chemokine/cytokines and insulin-dependent glucose uptake in human differentiated adipocytes. Methods Adipose tissues were obtained from patients undergoing liposuction. Stromal vascular cells were extracted and differentiated into adipocytes. A specific ligand for NOD1, was administered to human adipocytes in culture. Nuclear factor-κB transcriptional activity and proinflammatory chemokine/cytokines production were determined by reporter plasmid assay and enzyme-linked immunosorbent assay, respectively. Insulin-stimulated glucose uptake was measured by 2-deoxy-D-[ 3 H] glucose uptake assay. Furthermore, chemokine/cytokine secretion and glucose uptake in adipocytes transfected with small interfering RNA （siRNA） targeting NOD1 upon stimulation of NOD1 ligand were analyzed. Results Nuclear factor-κB transcriptional activity and monocyte chemoattractant protein-1 （MCP-1）, interleukin （IL）-6, and IL-8 secretion in human adipocytes were markedly increased stimulated with NOD1 ligand （all P〈0.01）. Insulin-induced glucose uptake was decreased upon the activation of NOD1 （P〈0.05）. NOD1 gene silencing by siRNA reduced NOD1 ligand-induced MCP-1, IL-6, and IL-8 release and increased insulin-induced glucose uptake （all P〈0.05）. Conclusion NOD1 activation in adipocytes might be implicated in the onset of insulin resistance.展开更多
文摘目的观察单核细胞趋化蛋白-1(MCP-1)、转化生长因子β_(1)(TGF-β_(1))、肿瘤坏死因子(TNF-α)在不同分期糖尿病肾病(DN)患者表达水平的差异,分析其与DN严重程度的相关性。方法选取2019年3月至2020年5月河南省人民医院收治的103例2型糖尿病(T2DM)患者,根据尿微量白蛋白排泄率(UAER)的差异将患者分为单纯T2DM组(24 h UAER<30 mg)35例、早期尿蛋白组(30 mg<24 h UAER<300 mg)36例,临床尿蛋白组(24 h UAER>300 mg)32例;选取同期在河南省人民医院进行体检的40例健康志愿者作为健康对照组。采集各组受检者血清样本,采用酶联免疫吸附法检测各组患者MCP-1、TGF-β_(1)、TNF-α水平;分析MCP-1、TGF-β_(1)、TNF-α水平与24 h UAEER的相关性。结果单纯T2DM组、早期尿蛋白组、临床尿蛋白组患者血清MCP-1、TGF-β_(1)、TNF-α水平高于健康对照组,差异有统计学意义(P<0.05);随着DN病情的不断加重,患者血清MCP-1、TGF-β_(1)、TNF-α水平随之升高。MCP-1、TGF-β_(1)、TNF-α在DN各阶段与UAER呈正相关(P<0.05)。结论MCP-1、TGF-β_(1)、TNF-α表达水平随着DN病情加重不断升高,检测MCP-1、TGF-β_(1)、TNF-α在患者血清中的表达水平可以作为判断DN疾病发展的重要指标。
文摘目的分析感染性休克患者血清炎症因子水平变化。方法选择2013年3月—2015年3月医院治疗的50例感染性休克患者作为观察组(n=50),并根据患者组患者在入院后是否发生多器官功能衰竭来分为发生组(n=21)及未发生组(n=29)。同期选取体检的50例健康人员作为对照组(n=50)。ELISA法检测血标本中血清趋化因子(CXCL-8)和单核细胞趋化蛋白1(MCP-1)的水平。结果发生组及未发生组患者血清CXCL-8及MCP-1水平明显高于对照组(CXCL-8, 6.02±0.54 vs. 1.02±0.22;4.33±0.38 vs. 1.02±0.22;MCP-1,201.33±28.13 vs. 20.62±10.62;170.12±30.31 vs. 20.62±10.62),对比差异均具有统计学意义(P <0.05);发生组患者血清CXCL-8及MCP-1水平明显高于未发生组(CXCL-8:6.02±0.54 vs. 4.33±0.38;MCP-1:201.33±28.13 vs. 170.12±30.31),两组间对比差异具有统计学意义(P <0.05)。结论感染性休克患者血清CXCL-8及MCP-1水平明显升高,且发生多器官功能衰竭的患者血清CXCL-8及MCP-1水平更高。临床上应密切关注感染性休克患者两种炎症因子变化,进而制定合理的治疗方案。
文摘Objective To investigate expression differences of neutrophil and mononuclear phagocyte related gene mRNAs among acute myocardial infarction （AMI）, stable angina （SA） and control groups, and then discuss their expression characteristics in the stable angina pectoris （SAP） and AMI stages of coronary artery disease （CAD）. Methods Whole Human Genome Oligo Microarrays were applied to assess the differential expression characteristics of neutrophil and mononuclear phagocyte related mRNAs in patients with AMI （n = 20）, SA （n = 20） and controls （n = 20）. Results （1） Almost all colony-stimulating factors （CSF） and their receptors related mRNAs was up-regulated in AMI and SA groups compared with the control group, and the expression of granulocyte-macrophage colony stimulating factor receptor （GM-CSFR） and granulocyte colony stimulating factor receptor （G-CSFR） mRNAs in the AMI group was significantly up-regulated compared with the other two groups （P 〈 0.01）. （2） The expression of mRNAs related to monocyte chemoattractant protein-1 （MCP-1）, CCR2 （MCP-1 receptor） and CXCR2 （IL-8 receptor） was significantly up-regulated （P 〈 0.01） in AMI group compared with SA and control groups IL-8 mRNA expression in the AMI group was clearly higher than the controls （P 〈 0.05）. （3） All mRNAs expression related to opsonic re- ceptors （IgG FoR and C3bR/C4bR） was significantly up-regulated in AMI group compared with SA and control group （P 〈 0.01）, and the SA group showed an upward trend compared with controls. （4） Most pattern recognition receptor （PRR）-related mRNAs expression was up-regulated in AMI group compared with SA and control groups. Most toll-like receptor （TLR） mRNAs expression was significantly up-regulated （P 〈 0.01） than the SA and control groups, macrophage scavenger receptor （MSR） mRNA was significantly up-regulated in AMI group compared with the control group （P 〈 0.01）, and the SA group showed an upward trend compared with the controls. Conclusions The expression of most neutrophil and mononuclear-macrophage function related genes mRNAs was significantly up-regulated by stages during the progression of CAD, suggesting that the adhesive, chemotactic and phagocytic functions of neutrophil and mononudear-macrophage were strengthened in the occurrence and development of coronary atherosclerosis and AMI. This also showed a stepped up- ward trend as the disease progressed.
文摘AIM:To investigate the effect of age on severity of acute pancreatitis(AP) using biochemical markers,histology and expression of the protective pancreatitisassociated proteins(PAPs).METHODS:AP was induced via intraductal injection of 4% sodium taurocholate in young and old rats.Sera and pancreata were assayed at 24 h for the parameters listed above;we also employed a novel molecular technique to assess bacterial infiltration using polymerase chain reaction to measure bacterial genomic ribosomal RNA.RESULTS:At 24 h after induction of AP,the pancreata of older animals had less edema(mean ± SE histologic score of young vs old:3.11 ± 0.16 vs 2.50 ±-0.11,P < 0.05),decreased local inflammatory response(histologic score of stromal infiltrate:3.11 ± 0.27 vs 2.00 ± 0.17,P < 0.05) and increased bacterial infiltration(174% ± 52% increase from sham vs 377% ± 4%,P < 0.05).A decreased expression of PAP1 and PAP2 was demonstrated by Western blotting analysis and immunohistochemical staining.There were no differences in serum amylase and lipase activity,or tissue myeloperoxidase or monocyte chemotactic protein-1 levels.However,in the most-aged group,serum C-reactive protein levels were higher(young vs old:0.249 ± 0.04 mg/dL vs 2.45 ± 0.68 mg/dL,P < 0.05).CONCLUSION:In older animals,there is depressed PAP expression related to a blunted inflammatory response in AP which is associated with worsened bacterial infiltration and higher C-reactive protein level;this may explain the more aggressive clinical course.
基金Supported by The Deanship of Scientific Research at King Saud University,through research group project,No.RGPVPP-016,entitled "Cardiovascular research Group"
文摘AIM:To investigate the effect of administration of agmatine(AGM) on gastric protection against ischemia reperfusion(I/R) injury.METHODS:Three groups of rats(6/group);sham,gastric I/R injury,and gastric I/R + AGM(100 mg/kg,i.p.given 15 min prior to gastric ischemia) were recruited.Gastric injury was conducted by ligating celiac artery for 30 min and reperfusion for another 30 min.Gastric tissues were histologically studied and immunostained with angiopoietin 1(Ang-1) and Ang-2.Vascular endothelial growth factor(VEGF) and monocyte chemoattractant protein-1(MCP-1) were measured in gastric tissue homogenate.To assess whether AKt/phosphatidyl inositol-3-kinase(PI3K) mediated the effect of AGM,an additional group was pretreated with Wortmannin(WM)(inhibitor of Akt/PI3K,15 μg/kg,i.p.),prior to ischemic injury and AGM treatment,and examined histologically and immunostained.Another set of experiments was run to study vascular permeability of the stomach using Evan's blue dye.RESULTS:AGM markedly reduced Evan's blue dye extravasation(3.58 ± 0.975 μg/stomach vs 1.175 ± 0.374 μg/stomach,P < 0.05),VEGF(36.87 ± 2.71 pg/100 mg protein vs 48.4 ± 6.53 pg/100 mg protein,P < 0.05) and MCP-1 tissue level(29.5 ± 7 pg/100 mg protein vs 41.17 ± 10.4 pg/100 mg protein,P < 0.01).It preserved gastric histology and reduced congestion.Ang-1 and Ang-2 immunostaining were reduced in stomach sections of AGM-treated animals.The administration of WM abolished the protective effects of AGM and extensive hemorrhage and ulcerations were seen.CONCLUSION:AGM protects the stomach against I/R injury by reducing vascular permeability and inflammation.This protection is possibly mediated by Akt/PI3K.
基金Supported by Grant from Department of Education of Liaoning Province(2008810)
文摘Objective To investigate the effects of stimulant for nucleotide-binding oligomerization domain 1 （NOD1） on secretion of proinflammatory chemokine/cytokines and insulin-dependent glucose uptake in human differentiated adipocytes. Methods Adipose tissues were obtained from patients undergoing liposuction. Stromal vascular cells were extracted and differentiated into adipocytes. A specific ligand for NOD1, was administered to human adipocytes in culture. Nuclear factor-κB transcriptional activity and proinflammatory chemokine/cytokines production were determined by reporter plasmid assay and enzyme-linked immunosorbent assay, respectively. Insulin-stimulated glucose uptake was measured by 2-deoxy-D-[ 3 H] glucose uptake assay. Furthermore, chemokine/cytokine secretion and glucose uptake in adipocytes transfected with small interfering RNA （siRNA） targeting NOD1 upon stimulation of NOD1 ligand were analyzed. Results Nuclear factor-κB transcriptional activity and monocyte chemoattractant protein-1 （MCP-1）, interleukin （IL）-6, and IL-8 secretion in human adipocytes were markedly increased stimulated with NOD1 ligand （all P〈0.01）. Insulin-induced glucose uptake was decreased upon the activation of NOD1 （P〈0.05）. NOD1 gene silencing by siRNA reduced NOD1 ligand-induced MCP-1, IL-6, and IL-8 release and increased insulin-induced glucose uptake （all P〈0.05）. Conclusion NOD1 activation in adipocytes might be implicated in the onset of insulin resistance.
