Subarachnoid hemorrhage is associated with high morbidity and mortality and lacks effective treatment.Pyroptosis is a crucial mechanism underlying early brain injury after subarachnoid hemorrhage.Previous studies have...Subarachnoid hemorrhage is associated with high morbidity and mortality and lacks effective treatment.Pyroptosis is a crucial mechanism underlying early brain injury after subarachnoid hemorrhage.Previous studies have confirmed that tumor necrosis factor-stimulated gene-6(TSG-6)can exert a neuroprotective effect by suppressing oxidative stress and apoptosis.However,no study to date has explored whether TSG-6 can alleviate pyroptosis in early brain injury after subarachnoid hemorrhage.In this study,a C57BL/6J mouse model of subarachnoid hemorrhage was established using the endovascular perforation method.Our results indicated that TSG-6 expression was predominantly detected in astrocytes,along with NLRC4 and gasdermin-D(GSDMD).The expression of NLRC4,GSDMD and its N-terminal domain(GSDMD-N),and cleaved caspase-1 was significantly enhanced after subarachnoid hemorrhage and accompanied by brain edema and neurological impairment.To explore how TSG-6 affects pyroptosis during early brain injury after subarachnoid hemorrhage,recombinant human TSG-6 or a siRNA targeting TSG-6 was injected into the cerebral ventricles.Exogenous TSG-6 administration downregulated the expression of NLRC4 and pyroptosis-associated proteins and alleviated brain edema and neurological deficits.Moreover,TSG-6 knockdown further increased the expression of NLRC4,which was accompanied by more severe astrocyte pyroptosis.In summary,our study revealed that TSG-6 provides neuroprotection against early brain injury after subarachnoid hemorrhage by suppressing NLRC4 inflammasome activation-induced astrocyte pyroptosis.展开更多
The levels of lipopolysaccharide (LPS) induced interleukin 6 (IL 6) and tumor necrosis factor α (TNF α) expression in culture of peripheral blood mononuclear cells (PBMC) and the plasma levels of IL 6 and TNF ...The levels of lipopolysaccharide (LPS) induced interleukin 6 (IL 6) and tumor necrosis factor α (TNF α) expression in culture of peripheral blood mononuclear cells (PBMC) and the plasma levels of IL 6 and TNF α in the patients with obstructive sleep apnea syndrome (OSAS) were measured and the relationship between OSAS and IL 6 or TNF α expression studied. Both IL 6 and TNF α were detected by using ELISA in 22 patients with OSAS and 16 normal controls. The levels of LPS induced IL 6 (787.82±151.97 pg/ml) and TNF α (4165.45±1501.43 pg/ml) expression in the supernatant of the culture of PBMC and plasma level of IL 6 (50.67±4.70 pg/ml) and TNF α (299.09±43.57 pg/ml) in the patients with OSAS were significantly higher than those in the normal controls (in the supernatant of the culture of PBMC: 562.69±197.54 pg/ml and 1596.25±403.08 pg/ml respectively; in the plasma: 12.69±2.75 pg/ml and 101.88±21.27 pg/ml respectively). There were significantly positive correlation between the levels of IL 6 and TNF α and the percentage of time of apnea and hyponea, as well as the percentage of time spending at SaO 2 below 90 % in the total sleep time. It was concluded that LPS induced IL 6 and TNF α levels as well as plasma IL 6 and TNF α levels in the patients with OSAS were up regulated, which may be associated with the pathogenesis of OSAS.展开更多
AIM: To evaluate the role of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in cirrhotic patients who have hepatic and renal impairment with spontaneous bacterial peritonitis (SBP).
BACKGROUND Inflammatory cytokines play a vital role in the occurrence of osteoarticular injury and inflammation. Whether inflammation-associated factors interleukin-1β(IL- 1β), IL-6, tumor necrosis factor-α(TNF-α)...BACKGROUND Inflammatory cytokines play a vital role in the occurrence of osteoarticular injury and inflammation. Whether inflammation-associated factors interleukin-1β(IL- 1β), IL-6, tumor necrosis factor-α(TNF-α) and vascular endothelial growth factor (VEGF) are involved in the pathogenesis of keen articular cartilage injury remains poorly understood. AIM To measure the levels of inflammatory factors [IL-1β, IL-6, TNF-α and VEGF] in patients with knee articular cartilage injury. METHODS Fifty-five patients with knee articular cartilage injury were selected as patient groups, who were divided into three grades [mild (n = 20), moderate (n = 19) and severe (n = 16)] according to disease severity and X-ray examinations. Meanwhile, 30 healthy individuals who underwent physical examination were selected as the control group. The levels of IL-1β, IL-6, TNF-α and VEGF were measured by ELISA and immunohistochemical staining. RESULTS Compared with the control group, patient groups displayed significantly higher levels of IL-1β, IL-6, TNF-α and VEGF, and the extent of increase was directly proportional to the severity of injury (P < 0.05). In addition, the number of cells with positive staining of IL-1β, IL-6, TNF-α and VEGF in the synovial membrane were significantly increased, along with increased disease severity (P < 0.05). After treatment, the scores of visual analogue scale and the Western Ontario and McMaster University of Orthopaedic Index in patient groups were 2.26 ± 1.13 and 15.56 ± 7.12 points, respectively, which were significantly lower than those before treatment (6.98 ± 1.32 and 49.48 ± 8.96). Correlation analysis suggested that IL-1β and TNF-α were positively correlated with VEGF. CONCLUSION IL-1β, IL-6, TNF-α and VEGF levels are increased in patients with knee articular cartilage injury, and are associated with the disease severity, indicating they might play an important role in the occurrence and development of knee articular cartilage injury. Furthermore, therapeutically targeting them might be a novel approach for the treatment of keen articular cartilage injury.展开更多
INTRODUCTIONDendritic cells (DCs) play a key regulatory role inantitumor immunity,especially in its immuneaccessory role via MHC-Ⅰ molecules.We haverecently reported that DCs were able to enhance thekilling activity ...INTRODUCTIONDendritic cells (DCs) play a key regulatory role inantitumor immunity,especially in its immuneaccessory role via MHC-Ⅰ molecules.We haverecently reported that DCs were able to enhance thekilling activity of Lymphokine and PHA activatedkiller (LPAK) cells in vitro.In the presentstudy,we evaluated the effects of GM-CSF andTNF upon antitumor activities of freshly展开更多
AIM: To investigate the effect of proinflammatory cytokine and an-ti-inflammatation cytokine on liver and lung tissues in rats with endotoxemi-a. METHODS: Male Wistar rats were randomly divided into 4 groups: group tr...AIM: To investigate the effect of proinflammatory cytokine and an-ti-inflammatation cytokine on liver and lung tissues in rats with endotoxemi-a. METHODS: Male Wistar rats were randomly divided into 4 groups: group treated with stimulating vagus nerve, group receiving lipopolysaccharide (LPS) intravenous injection after transecting vagus nerve, group treated with sham operation and group treated with injecting LPS intravenously alone, and then measured the levels of TNF-αin liver and lung and those of cortisol and Alanine aminotransferase (ALT) in plasma. RESULTS: Compared with group treated with sham operation, LPS-treated groups showed a significant increase in TNF level, which was at most 15 fold higher than that of the former group. There was a significant decease in TNF level in group treated with stimulating vagus nerve, compared with both group receiving LPS intravenous injection after transecting vagous nerve and group treated only with LPS. In addition, we observed plasma cortisol level in LPS-treated group was much higher than other 3 groups and the plasma ALT level was greatly lower than that of group treated only with LPS. CONCLUSION: Stimulating vagous nerve can significantly decrease the production of proinflammatory cytokine and alleviate inflammation in rats with endotoxemia.展开更多
Tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) are involved in the progression of coronary artery disease (CAD). The cytokines’ levels are associated with the severity of CAD. We have recently repor...Tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) are involved in the progression of coronary artery disease (CAD). The cytokines’ levels are associated with the severity of CAD. We have recently reported on the association of resistin, a relatively novel cytokine with the pathogenesis of cardiovascular disease (CVD). Although the inflammatory cytokines’ impact on atherosclerosis is widely accepted, yet some controversy exists regarding the involvement of these factors in atherogenesis. The current review highlights the potential association of TNF-alpha, IL-6 and resistin SNPs (single nucleotide polymorphisms) with CAD. Molecular genetics data along with the intracellular signaling cascade mechanisms may have important clinical implications in the treatment of CAD.展开更多
目的研究孕早期妇女血清补体C1q/肿瘤坏死因子相关蛋白6(C1q/tumor necrosis factor-related protein 6,CTRP6)的表达水平,探讨其与妊娠糖尿病(gestational diabetes mellitus,GDM)的关系。方法前瞻性连续选取2021年3月至2022年3月在郑...目的研究孕早期妇女血清补体C1q/肿瘤坏死因子相关蛋白6(C1q/tumor necrosis factor-related protein 6,CTRP6)的表达水平,探讨其与妊娠糖尿病(gestational diabetes mellitus,GDM)的关系。方法前瞻性连续选取2021年3月至2022年3月在郑州大学第二附属医院门诊产检的孕10~13周孕妇,收集孕妇的年龄、身高、体质量、末次月经时间,检测孕早期总胆固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)、高密度脂蛋白(high density lipoprotein,HDL)、低密度脂蛋白(low density lipoprotein,LDL)、空腹血糖(fasting plasma glucose,FPG)、糖化血红蛋白(glycosylated hemoglobin,HbA1c)、空腹胰岛素(fasting insulin,FINS)、CTRP6水平,计算孕前体质量指数(body mass index,BMI)、基线BMI、产前BMI和胰岛素抵抗指数(亦称胰岛素抵抗的稳态模型评估,homeostatic model assessment of insulin resistance,HOMA-IR)。所有孕妇均于孕24~28周行75g口服葡萄糖耐量试验,根据试验结果分为GDM组和糖耐量正常(normal glucose tolerance,NGT)组。比较两组孕妇孕早期的临床资料及实验室指标,分析孕早期血清CTRP6与各指标的相关性及其与GDM的关系。结果共纳入孕妇213例,完整随访203例,其中52例孕妇被诊断为GDM,GDM发病率25.62%。GDM组孕妇的孕早期血清CTRP6、年龄、孕前BMI、基线BMI、产前BMI、TC、LDL、FPG、HbA1c、FINS、HOMA-IR均较NGT组升高,差异有统计学意义(P<0.05)。孕早期CTRP6与年龄、孕前BMI、基线BMI、产前BMI、TG、LDL、FPG、HbA1c、FINS、HOMA-IR呈正相关,与HDL呈负相关(P<0.05)。校正年龄、BMI、糖脂代谢指标及HOMA-IR后,孕早期CTRP6为GDM发病的独立影响因素。结论孕早期血清CTRP6升高与GDM相关,是GDM的独立危险因素。展开更多
目的:检测急性心肌梗死(acute myocardial infarction,AMI)患者血清C1q/肿瘤坏死因子相关蛋白-6(C1q/tumor necrosis factor related protein 6,CTRP6)表达水平与病情和预后的相关性。方法:选取河南科技大学第一附属医院2021年1月至2022...目的:检测急性心肌梗死(acute myocardial infarction,AMI)患者血清C1q/肿瘤坏死因子相关蛋白-6(C1q/tumor necrosis factor related protein 6,CTRP6)表达水平与病情和预后的相关性。方法:选取河南科技大学第一附属医院2021年1月至2022年1月收治的144例AMI患者为研究对象,检测血清CTRP6的表达含量,并分析及评估CTRP6表达与AMI患者的临床特征和MACE的相关性。结果:AMI组患者外周血CTRP6含量为119.32(78.4,165.8)μg/L,显著低于对照组的372.3(303.6,454.2)μg/L(P<0.05);与高表达组比较,低表达组患者血清CK-MB、NT-proBNP、Gensini评分和SYNTAX II评分明显升高(P<0.05),而LVEF明显降低(P<0.05);此外,CTRP6低表达组患者MACE的累积发生率显著高于CTRP6高表达组(P<0.05);CTRP6预测AMI患者发生MACE事件的ROC曲线下面积为0.851。当最佳截断值为当88.423μg/L时,此时的敏感性为75.3%,特异性87.4%。结论:AMI患者血清CTRP6的表达明显降低,且CTRP6低表达可能是识别AMI高危患者和优化治疗策略的重要靶点。展开更多
基金supported the National Natural Science Foundation of China,No.81974178(to CD).
文摘Subarachnoid hemorrhage is associated with high morbidity and mortality and lacks effective treatment.Pyroptosis is a crucial mechanism underlying early brain injury after subarachnoid hemorrhage.Previous studies have confirmed that tumor necrosis factor-stimulated gene-6(TSG-6)can exert a neuroprotective effect by suppressing oxidative stress and apoptosis.However,no study to date has explored whether TSG-6 can alleviate pyroptosis in early brain injury after subarachnoid hemorrhage.In this study,a C57BL/6J mouse model of subarachnoid hemorrhage was established using the endovascular perforation method.Our results indicated that TSG-6 expression was predominantly detected in astrocytes,along with NLRC4 and gasdermin-D(GSDMD).The expression of NLRC4,GSDMD and its N-terminal domain(GSDMD-N),and cleaved caspase-1 was significantly enhanced after subarachnoid hemorrhage and accompanied by brain edema and neurological impairment.To explore how TSG-6 affects pyroptosis during early brain injury after subarachnoid hemorrhage,recombinant human TSG-6 or a siRNA targeting TSG-6 was injected into the cerebral ventricles.Exogenous TSG-6 administration downregulated the expression of NLRC4 and pyroptosis-associated proteins and alleviated brain edema and neurological deficits.Moreover,TSG-6 knockdown further increased the expression of NLRC4,which was accompanied by more severe astrocyte pyroptosis.In summary,our study revealed that TSG-6 provides neuroprotection against early brain injury after subarachnoid hemorrhage by suppressing NLRC4 inflammasome activation-induced astrocyte pyroptosis.
文摘The levels of lipopolysaccharide (LPS) induced interleukin 6 (IL 6) and tumor necrosis factor α (TNF α) expression in culture of peripheral blood mononuclear cells (PBMC) and the plasma levels of IL 6 and TNF α in the patients with obstructive sleep apnea syndrome (OSAS) were measured and the relationship between OSAS and IL 6 or TNF α expression studied. Both IL 6 and TNF α were detected by using ELISA in 22 patients with OSAS and 16 normal controls. The levels of LPS induced IL 6 (787.82±151.97 pg/ml) and TNF α (4165.45±1501.43 pg/ml) expression in the supernatant of the culture of PBMC and plasma level of IL 6 (50.67±4.70 pg/ml) and TNF α (299.09±43.57 pg/ml) in the patients with OSAS were significantly higher than those in the normal controls (in the supernatant of the culture of PBMC: 562.69±197.54 pg/ml and 1596.25±403.08 pg/ml respectively; in the plasma: 12.69±2.75 pg/ml and 101.88±21.27 pg/ml respectively). There were significantly positive correlation between the levels of IL 6 and TNF α and the percentage of time of apnea and hyponea, as well as the percentage of time spending at SaO 2 below 90 % in the total sleep time. It was concluded that LPS induced IL 6 and TNF α levels as well as plasma IL 6 and TNF α levels in the patients with OSAS were up regulated, which may be associated with the pathogenesis of OSAS.
文摘AIM: To evaluate the role of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in cirrhotic patients who have hepatic and renal impairment with spontaneous bacterial peritonitis (SBP).
文摘BACKGROUND Inflammatory cytokines play a vital role in the occurrence of osteoarticular injury and inflammation. Whether inflammation-associated factors interleukin-1β(IL- 1β), IL-6, tumor necrosis factor-α(TNF-α) and vascular endothelial growth factor (VEGF) are involved in the pathogenesis of keen articular cartilage injury remains poorly understood. AIM To measure the levels of inflammatory factors [IL-1β, IL-6, TNF-α and VEGF] in patients with knee articular cartilage injury. METHODS Fifty-five patients with knee articular cartilage injury were selected as patient groups, who were divided into three grades [mild (n = 20), moderate (n = 19) and severe (n = 16)] according to disease severity and X-ray examinations. Meanwhile, 30 healthy individuals who underwent physical examination were selected as the control group. The levels of IL-1β, IL-6, TNF-α and VEGF were measured by ELISA and immunohistochemical staining. RESULTS Compared with the control group, patient groups displayed significantly higher levels of IL-1β, IL-6, TNF-α and VEGF, and the extent of increase was directly proportional to the severity of injury (P < 0.05). In addition, the number of cells with positive staining of IL-1β, IL-6, TNF-α and VEGF in the synovial membrane were significantly increased, along with increased disease severity (P < 0.05). After treatment, the scores of visual analogue scale and the Western Ontario and McMaster University of Orthopaedic Index in patient groups were 2.26 ± 1.13 and 15.56 ± 7.12 points, respectively, which were significantly lower than those before treatment (6.98 ± 1.32 and 49.48 ± 8.96). Correlation analysis suggested that IL-1β and TNF-α were positively correlated with VEGF. CONCLUSION IL-1β, IL-6, TNF-α and VEGF levels are increased in patients with knee articular cartilage injury, and are associated with the disease severity, indicating they might play an important role in the occurrence and development of knee articular cartilage injury. Furthermore, therapeutically targeting them might be a novel approach for the treatment of keen articular cartilage injury.
基金Natural Science Foundation of the Higher Education Office of Guangdong Province,No.19952901
文摘INTRODUCTIONDendritic cells (DCs) play a key regulatory role inantitumor immunity,especially in its immuneaccessory role via MHC-Ⅰ molecules.We haverecently reported that DCs were able to enhance thekilling activity of Lymphokine and PHA activatedkiller (LPAK) cells in vitro.In the presentstudy,we evaluated the effects of GM-CSF andTNF upon antitumor activities of freshly
基金Supported by the National Military Medical Science Fundation of the Tenth Five-year Plan.(No.01L081)
文摘AIM: To investigate the effect of proinflammatory cytokine and an-ti-inflammatation cytokine on liver and lung tissues in rats with endotoxemi-a. METHODS: Male Wistar rats were randomly divided into 4 groups: group treated with stimulating vagus nerve, group receiving lipopolysaccharide (LPS) intravenous injection after transecting vagus nerve, group treated with sham operation and group treated with injecting LPS intravenously alone, and then measured the levels of TNF-αin liver and lung and those of cortisol and Alanine aminotransferase (ALT) in plasma. RESULTS: Compared with group treated with sham operation, LPS-treated groups showed a significant increase in TNF level, which was at most 15 fold higher than that of the former group. There was a significant decease in TNF level in group treated with stimulating vagus nerve, compared with both group receiving LPS intravenous injection after transecting vagous nerve and group treated only with LPS. In addition, we observed plasma cortisol level in LPS-treated group was much higher than other 3 groups and the plasma ALT level was greatly lower than that of group treated only with LPS. CONCLUSION: Stimulating vagous nerve can significantly decrease the production of proinflammatory cytokine and alleviate inflammation in rats with endotoxemia.
文摘Tumor necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) are involved in the progression of coronary artery disease (CAD). The cytokines’ levels are associated with the severity of CAD. We have recently reported on the association of resistin, a relatively novel cytokine with the pathogenesis of cardiovascular disease (CVD). Although the inflammatory cytokines’ impact on atherosclerosis is widely accepted, yet some controversy exists regarding the involvement of these factors in atherogenesis. The current review highlights the potential association of TNF-alpha, IL-6 and resistin SNPs (single nucleotide polymorphisms) with CAD. Molecular genetics data along with the intracellular signaling cascade mechanisms may have important clinical implications in the treatment of CAD.
文摘目的研究孕早期妇女血清补体C1q/肿瘤坏死因子相关蛋白6(C1q/tumor necrosis factor-related protein 6,CTRP6)的表达水平,探讨其与妊娠糖尿病(gestational diabetes mellitus,GDM)的关系。方法前瞻性连续选取2021年3月至2022年3月在郑州大学第二附属医院门诊产检的孕10~13周孕妇,收集孕妇的年龄、身高、体质量、末次月经时间,检测孕早期总胆固醇(total cholesterol,TC)、三酰甘油(triglyceride,TG)、高密度脂蛋白(high density lipoprotein,HDL)、低密度脂蛋白(low density lipoprotein,LDL)、空腹血糖(fasting plasma glucose,FPG)、糖化血红蛋白(glycosylated hemoglobin,HbA1c)、空腹胰岛素(fasting insulin,FINS)、CTRP6水平,计算孕前体质量指数(body mass index,BMI)、基线BMI、产前BMI和胰岛素抵抗指数(亦称胰岛素抵抗的稳态模型评估,homeostatic model assessment of insulin resistance,HOMA-IR)。所有孕妇均于孕24~28周行75g口服葡萄糖耐量试验,根据试验结果分为GDM组和糖耐量正常(normal glucose tolerance,NGT)组。比较两组孕妇孕早期的临床资料及实验室指标,分析孕早期血清CTRP6与各指标的相关性及其与GDM的关系。结果共纳入孕妇213例,完整随访203例,其中52例孕妇被诊断为GDM,GDM发病率25.62%。GDM组孕妇的孕早期血清CTRP6、年龄、孕前BMI、基线BMI、产前BMI、TC、LDL、FPG、HbA1c、FINS、HOMA-IR均较NGT组升高,差异有统计学意义(P<0.05)。孕早期CTRP6与年龄、孕前BMI、基线BMI、产前BMI、TG、LDL、FPG、HbA1c、FINS、HOMA-IR呈正相关,与HDL呈负相关(P<0.05)。校正年龄、BMI、糖脂代谢指标及HOMA-IR后,孕早期CTRP6为GDM发病的独立影响因素。结论孕早期血清CTRP6升高与GDM相关,是GDM的独立危险因素。
文摘目的:检测急性心肌梗死(acute myocardial infarction,AMI)患者血清C1q/肿瘤坏死因子相关蛋白-6(C1q/tumor necrosis factor related protein 6,CTRP6)表达水平与病情和预后的相关性。方法:选取河南科技大学第一附属医院2021年1月至2022年1月收治的144例AMI患者为研究对象,检测血清CTRP6的表达含量,并分析及评估CTRP6表达与AMI患者的临床特征和MACE的相关性。结果:AMI组患者外周血CTRP6含量为119.32(78.4,165.8)μg/L,显著低于对照组的372.3(303.6,454.2)μg/L(P<0.05);与高表达组比较,低表达组患者血清CK-MB、NT-proBNP、Gensini评分和SYNTAX II评分明显升高(P<0.05),而LVEF明显降低(P<0.05);此外,CTRP6低表达组患者MACE的累积发生率显著高于CTRP6高表达组(P<0.05);CTRP6预测AMI患者发生MACE事件的ROC曲线下面积为0.851。当最佳截断值为当88.423μg/L时,此时的敏感性为75.3%,特异性87.4%。结论:AMI患者血清CTRP6的表达明显降低,且CTRP6低表达可能是识别AMI高危患者和优化治疗策略的重要靶点。
文摘胎儿生长受限(fetal growth restriction,FGR)是一种常见的产科疾病,其可导致新生儿低出生体质量和出生后肌肉量减少。这可能与肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)和白细胞介素-6(interleukin-6,IL-6)的调控密切相关。研究发现,这两种炎症因子在FGR胎儿中表达水平异常,可通过影响成肌细胞的增殖和分化,干扰正常骨骼肌的发育。此外,TNF-α与IL-6还可以激活特定的信号通路,如核因子κB(nuclear factor-κB,NF-κB)、Janus激酶/信号转导及转录活化因子(Janus kinase/signal transducer and activator of transcription,JAK/STAT)、丝裂原激活的蛋白激酶(mitogen-activated protein kinase,MAPK)等信号通路,调节肌细胞的代谢和功能。如使用特定的抗炎药物或生物制剂来降低TNF-α和IL-6的活性,可能有助于改善FGR胎儿的骨骼肌发育。总的来说,TNF-α和IL-6在FGR胎儿骨骼肌发育中的作用是一个多层面、复杂的过程,需要进一步的深入研究来阐明其具体机制,帮助理解FGR的病理生理学,并为治疗FGR胎儿提供新的思路。
