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β-紫罗兰酮通过NF-κB途径抑制乳腺癌细胞增殖
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作者 高光强 王发琳 +5 位作者 李娟 田虹 果思伽 于晓兰 杨婷婷 刘家仁 《实用肿瘤学杂志》 CAS 2024年第4期254-261,共8页
目的探讨β-紫罗兰酮(β-Ionone,BI)通过调节核因子-κB(Nuclear factor kappa-B,NF-κB)对乳腺癌细胞增殖过程的抑制作用及其可能的机制。方法采用亚甲基蓝(Methylene blue,MB)法和MTT法测定人乳腺癌BT549细胞和MCF-7细胞活性,孔雀石... 目的探讨β-紫罗兰酮(β-Ionone,BI)通过调节核因子-κB(Nuclear factor kappa-B,NF-κB)对乳腺癌细胞增殖过程的抑制作用及其可能的机制。方法采用亚甲基蓝(Methylene blue,MB)法和MTT法测定人乳腺癌BT549细胞和MCF-7细胞活性,孔雀石绿磷酸盐法检测蛋白磷酸酶2A(Protein phosphatase 2A,PP2A)活性、免疫印迹法检测磷酸化P65(p-P65)(s536和s311)、PP2A(A、B和C)和磷酸化共济失调毛细血管扩张突变基因(Phosphorylation-ataxia telangiectasia-mutated gene,p-ATM)(s1981)蛋白水平。结果BI可明显抑制人乳腺癌BT549细胞和MCF-7细胞的增殖,且呈时间和剂量依赖性,差异具有统计学意义(P<0.01)。MCF-7细胞经BI处理后,NF-κB活性被显著抑制,表现为磷酸化P65(s536和s311)的蛋白水平显著降低,PP2A的蛋白水平升高,差异具有统计学意义(P<0.05)。此外,BI还显著地降低PP2A抑制剂冈田酸(Okadaic acid,OA)对MCF-7细胞中P65蛋白和ATM蛋白的磷酸化作用。结论该研究表明BI通过抑制NF-κB活性来抑制乳腺癌细胞的增殖,其机制可能是BI通过增加PP2A活性调节NF-κB通路。 展开更多
关键词 乳腺癌 Β-紫罗兰酮 蛋白磷酸酶2A 核因子-Κb 共济失调毛细血管扩张突变基因
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创伤性脑损伤患者血清AQP4和NF-κB p65表达与神经功能缺损程度及预后的关系
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作者 朱刚毅 朱义通 陆兆丰 《海南医学》 CAS 2024年第7期934-938,共5页
目的探讨创伤性脑损伤(TBI)患者血清水通道蛋白4(AQP4)和核因子κB(NF-κB p65)表达与神经功能缺损程度及预后的关系。方法选取2021年3月至2023年3月于河南科技大学第一附属医院开元急诊科收治的128例TBI患者作为研究对象(观察组),根据... 目的探讨创伤性脑损伤(TBI)患者血清水通道蛋白4(AQP4)和核因子κB(NF-κB p65)表达与神经功能缺损程度及预后的关系。方法选取2021年3月至2023年3月于河南科技大学第一附属医院开元急诊科收治的128例TBI患者作为研究对象(观察组),根据美国国立卫生院神经缺损评估量表(NIHSS)将患者分为重度组31例、中度组45例和轻度组52例;根据格拉斯哥预后量表(GOS)评分将患者分为预后不良组37例和预后良好组91例。另选取同期于本院体检的128例健康志愿者作为对照组。比较各组受检者的一般资料及血清AQP4和NF-κB p65水平,采用Spearman法分析血清AQP4、NF-κB p65水平与NIHSS评分的相关性,采用受试者工作特征曲线(ROC)分析血清AQP4、NF-κB p65对TBI患者预后不良的预测价值。结果观察组患者的血清AQP4、NF-κB p65水平分别为(27.37±6.34)μg/L、(2.27±0.24)ng/mL,明显高于对照组的(12.65±3.21)μg/L、(0.36±0.11)ng/mL,差异均具有统计学意义(P<0.05)。Spearman相关性分析结果显示,TBI患者血清AQP4、NF-κB p65水平与NIHSS评分均呈正相关(r=0.605、0.612,P<0.05)。入院24 h血清AQP4、NF-κB p65水平比较,重度组>中度组>轻度组,48 h、72 h有同样的趋势,差异均具有统计学意义(P<0.05)。预后不良组患者的血清AQP4、NF-κB p65水平分别为(34.65±7.51)μg/L、(2.71±0.40)ng/mL,明显高于预后良好组的(24.41±6.48)μg/L、(2.09±0.22)ng/mL,差异均有统计学意义(P<0.05)。血清AQP4、NF-κB p65两者联合预测TBI患者预后不良的曲线下面积(AUC)为0.938,高于各单一指标的0.873、0.830,联合预测的敏感度为91.89%,特异度为85.71%,两者联合优于血清AQP4、NF-κB p65各自单独预测(Z两者联合-AQP4=2.564、Z两者联合-NF-κB p65=2.555,P=0.010、0.011)。结论TBI患者血清AQP4、NF-κB p65水平上升与神经功能缺损程度和不良预后有关,可作为预测预后的潜在标志物。 展开更多
关键词 创伤性脑损伤 水通道蛋白4 核因子κb 神经功能缺损 预后
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Delayed hepatocarcinogenesis through antiangiogenic intervention in the nuclear factor-kappa B activation pathway in rats 被引量:31
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作者 Dong, Zhi-Zhen Yao, Deng-Fu +7 位作者 Wu, Wei Yao, Min Yu, Hong-Bo Shen, Jun-Jun Qiu, Li-Wei Yao, Ning-Hua Sai, Wen-Li Yang, Jun-Ling 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2010年第2期169-174,共6页
BACKGROUND: The active form of nuclear factor-kappa B (NF-kappa B) is involved in the initiation, generation, and development of hepatocellular carcinoma (HCC), and is up-regulated in inflammation-associated malignanc... BACKGROUND: The active form of nuclear factor-kappa B (NF-kappa B) is involved in the initiation, generation, and development of hepatocellular carcinoma (HCC), and is up-regulated in inflammation-associated malignancies. We investigated the dynamic expression of NF-kappa B and its influences on the occurrence of HCC through antiangiogenic (thalidomide) intervention in NF-kappa B activation. METHODS : Hepatoma models were induced with 2-fluorenylacetamide (2-FAA, 0.05%) in male Sprague-Dawley rats, and thalidomide (100 mg/kg body weight) was administered intragastrically to intervene in NF-kappa B activation. The pathological changes in the liver of sacrificed rats were assessed after hematoxylin and eosin staining. NF-kappa B mRNA was amplified by RT-nested PCR. The alterations of NF-kappa B and vascular endothelial growth factor (VEGF) expression were analyzed by enzyme-linked immunosorbent assay, immunohistochemistry, and Western blotting. RESULTS: Rat hepatocytes showed denatured, precancerous, and cancerous stages in hepatocarcinogenesis, with an increasing tendency of hepatic NF-kappa B, NF-kappa B mRNA, and VEGF expression, and their values in the HCC group were higher than those in controls (P<0.001). In the thalidomide-treated group, the morphologic changes generated only punctiform denaturation and necrosis at the early or middle stages, and nodular hyperplasia or a little atypical hyperplasia at the final stages, with the expression of NF-kappa B (chi(2)=9.93, P<0.001) and VEGF (chi(2)=8.024, P<0.001) lower than that in the 2-FAA group. CONCLUSION: NF-kappa B is overexpressed in hepatocarcinogenesis and antiangiogenic treatment down-regulates the expression of NF-kappa B and VEGF, and delays the occurrence of HCC. (Hepatobiliary Pancreat Dis Int 2010; 9: 169-174) 展开更多
关键词 hepatocellular carcinoma nuclear factor-kappa b vascular endothelial growth factor INTERVENTION dynamic expression
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Urinary trypsin inhibitor attenuates hepatic ischemia-reperfusion injury by reducing nuclear factor-kappa B activation 被引量:28
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作者 Wu, Yi-Jun Ling, Qi +4 位作者 Zhou, Xin-Hui Wang, Yan Xie, Hai-Yang Yu, Ji-Ren Zheng, Shu-Sen 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2009年第1期53-58,共6页
BACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa B (NF-kappa B) and i... BACKGROUND: Urinary trypsin inhibitor (UTI) inhibits the inflammatory response and protects against ischemia-reperfusion (I/R) injury. The inflammatory response is mediated by nuclear factor-kappa B (NF-kappa B) and its related target genes and products such as vascular endothelial cell adhesion molecule and CXC chemokines. We aimed to assess the roles of those mediators in a UTI-treated mouse model of hepatic I/R injury. METHODS: Treatment group 1 (UTI given 5 minutes prior to liver ischemia), treatment group 2 (UTI given 5 minutes after the anhepatic phase) and a control group were investigated. Blood and liver samples were obtained and compared at 1, 3, 6 and 24 hours after reperfusion. RESULTS: Attenuation of pathological hepatocellular damage was greater in the treatment groups than in the control group (P < 0.05). Compared with the control group, the UTI treatment groups showed significantly lower serum alanine aminotransferase and aspartate aminotransferase levels, decreased myeloperoxidase activity, and reduced NF-kappa B activation. Also downregulated was the expression of tumor necrosis factor-alpha, cytokine-induced neutrophil chemoattractant, and macrophage inflammatory protein-2 at the mRNA level. P-selectin protein and intercellular adhesion molecule-1 protein expression were also downregulated. In addition, the treatment group I showed a better protective effect against I/R injury than the treatment group 2. CONCLUSIONS: UTI reduces NF-kappa B activation and downregulates the expression of its related mediators, followed by the inhibition of neutrophil aggregation and infiltration in hepatic I/R injury. The protective role of UTI is more effective in prevention than in treatment. 展开更多
关键词 ischemia-reperfusion injury nuclear factor-kappa b tumor necrosis factor-alpha urinary trypsin inhibitor
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Characteristics of hepatic nuclear-transcription factor-kappa B expression and quantitative analysis in rat hepatocarcinogenesis 被引量:12
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作者 Wu, Wei Yao, Deng-Fu +7 位作者 Qiu, Li-Wei Sai, Wen-Li Shen, Jun-Jun Yu, Hong-Bo Wu, Xin-Hua Li, Yue-Ming Wang, Yi-Lang Gu, Wen-Jing 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2009年第5期504-509,共6页
BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. We analyzed the expression of miclear-transcription factor-kappa B (NF-kappa B) during hepatocarcinogenesis in order to evaluate i... BACKGROUND: Hepatocellular carcinoma (HCC) is one of the most common malignant tumors. We analyzed the expression of miclear-transcription factor-kappa B (NF-kappa B) during hepatocarcinogenesis in order to evaluate its dynamic expression and its clinical value in the development and diagnosis of HCC. METHODS: Hepatoma models were induced by oral administration of 2-acetamidoflurene (2-FAA) to male Sprague-Dawley rats. Morphological changes were observed after hematoxylin and eosin staining. The cellular distribution of NF-kappa B expression during different stages of cancer development was investigated by immunohistochemistry, and the level of NF-kappa B expression in liver tissues was quantitatively analyzed by ELISA. The gene fragments of hepatic NF-kappa B were amplified by nested-polymerase chain reaction assay. RESULTS: Hepatocytes showed vacuole-like degeneration during the early stages, then had a hyperplastic nodal appearance during the middle stages, and finally progressed to tubercles of cancerous nests with high differentiation. The NF-kappa B-positive material was buff-colored, fine particles localized in the nucleus, and the incidence of NF-kappa B-positive cells was 81.8% in degeneration, 83.3% in precancerous lesions, and 100% in cancerous tissues. All of these values were higher than those in controls (P<0.01). Hepatic NF-kappa B expression and hepatic NF-kappa B-mRNA were also higher during the course of HCC development (P<0.01). CONCLUSION: The NF-kappa B signal transduction pathway is activated during the early stages of HCC development, and its abnormal expression may be associated with the occurrence of HCC. 展开更多
关键词 hepatocellular carcinoma nuclear factor-kappa b IMMUNOHISTOCHEMISTRY nested-polymerase chain reaction NF-kappa b-mRNA
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Atsttrin reduces lipopolysaccharide-induced neuroinflammation by inhibiting the nuclear factor kappa B signaling pathway 被引量:3
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作者 Lian Liu Yuan Qu +7 位作者 Yi Liu Hua Zhao He-Cheng Ma Ahmed Fayyaz Noor Chang-Jiao Ji Lin Nie Meng Si Lei Cheng 《Neural Regeneration Research》 SCIE CAS CSCD 2019年第11期1994-2002,共9页
Progranulin is closely related to neuronal survival in a neuroinflammatory mouse model and attenuates inflammatory reactions. Atsttrin is an engineered protein composed of three progranulin fragments and has been show... Progranulin is closely related to neuronal survival in a neuroinflammatory mouse model and attenuates inflammatory reactions. Atsttrin is an engineered protein composed of three progranulin fragments and has been shown to have an effect similar to that of progranulin. Atsttrin has anti-inflammatory actions in multiple arthritis mouse models, and it protects against further arthritis development. However, whether Atsttrin has a role in neuroinflammation remains to be elucidated. In this study, we produced a neuroinflammatory mouse model by intracerebroventricular injection of 1 μL lipopolysaccharide(10 μg/μL). Atsttrin(2.5 mg/kg) was administered via intraperitoneal injection every 3 days over a period of 7 days before intracerebroventricular injection of 1 μL lipopolysaccharide(10 μg/μL). In addition, astrocyte cultures were treated with 0, 100 or 300 ng/mL lipopolysaccharide, with 200 ng/mL Atsttrin simultaneously. Immunohistochemistry, enzyme-linked immunosorbent assay and real-time reverse transcription-polymerase chain reaction were performed to examine the protein and mRNA levels of inflammatory mediators and to assess activation of the nuclear factor kappa B signaling pathway. Progranulin expression in the brain of wild-type mice and in astrocyte cultures was increased after lipopolysaccharide administration. The protein and mRNA expression levels of tumor necrosis factor-α, interleukin-1β and inducible nitric oxide synthase were increased in the brain of progranulin knockout mice after lipopolysaccharide administration. Atsttrin treatment reduced the lipopolysaccharide-induced increase in the protein and mRNA levels of tumor necrosis factor-α, interleukin-1β, matrix metalloproteinase-3 and inducible nitric oxide synthase in the brain of progranulin knockout mice. Atsttrin also reduced the expression of cyclooxygenase-2, inducible nitric oxide synthase and matrix metalloproteinase 3 mRNA in lipopolysaccharide-treated astrocytes in vitro, and decreased the concentration of tumor necrosis factor α and interleukin-1β in the supernatant. Furthermore, Atsttrin significantly reduced the levels of phospho-nuclear factor kappa B inhibitor α in the brain of lipopolysaccharide-treated progranulin knockout mice and astrocytes, and it decreased the expression of nuclear factor kappa B2 in astrocytes. Collectively, our findings show that the anti-neuroinflammatory effect of Atsttrin involves inhibiton of the nuclear factor kappa B signaling pathway, and they suggest that Atsttrin may have clinical potential in neuroinflammatory therapy. 展开更多
关键词 nerve REGENERATION progranulin Atsttrin NEUROINFLAMMATION inflammatory cytokines LIPOPOLYSACCHARIDE INTRACEREbROVENTRICULAR injection astrocyte nuclear factor kappa b signaling pathway progranulin KNOCKOUT mouse CEREbROSPINAL fluid neural REGENERATION
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Up-regulation of intestinal nuclear factor kappa B and intercellular adhesion molecule-1 following traumatic brain injury in rats 被引量:16
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作者 Chun-HuaHang Ji-XinShi +2 位作者 Jie-ShouLi Wei-QinLi Hong-XiaYin 《World Journal of Gastroenterology》 SCIE CAS CSCD 2005年第8期1149-1154,共6页
AIM: Nuclear factor kappa B (NF-κB) regulates a large number of genes involved in the inflammatory response to critical illnesses, but it is not known if and how NF-KB is activated and intercellular adhesion molecule... AIM: Nuclear factor kappa B (NF-κB) regulates a large number of genes involved in the inflammatory response to critical illnesses, but it is not known if and how NF-KB is activated and intercellular adhesion molecule-1 (ICAM-1) expressed in the gut following traumatic brain injury (TBI). The aim of current study was to investigate the temporal pattern of intestinal NF-κB activation and ICAM-1 expression following TBI. METHODS: Male Wistar rats were randomly divided into six groups (6 rats in each group) including controls with sham operation and TBI groups at hours 3, 12, 24, and 72, and on d 7. Parietal brain contusion was adopted using weight-dropping method. All rats were decapitated at corresponding time point and mid-jejunum samples were taken. NF-KB binding activity in jejunal tissue was measured using EMSA. Immunohistochemistry was used for detection of ICAM-1 expression in jejunal samples. RESULTS: There was a very low NF-κB binding activity and little ICAM-1 expression in the gut of control rats after sham surgery. NF-KB binding activity in jejunum significantly increased by 160% at 3 h following TBI (P<0.05 vs control), peaked at 72 h (500% increase) and remained elevated on d 7 post-injury by 390% increase. Compared to controls, ICAM-1 was significantly up-regulated on the endothelia of microvessels in villous interstitium and lamina propria by 24 h following TBI and maximally expressed at 72 h post-injury (P<0.001). The endothelial ICAM-1 immunoreactivity in jejunal mucosa still remained strong on d 7 post-injury. The peak of NF-κB activation and endothelial ICAM-1 expression coincided in time with the period during which secondary mucosal injury of the gut was also at their culmination following TBI. CONCLUSION: TBI could induce an immediate and persistent up-regulation of NF-κB activity and subsequent up-regulation of ICAM-1 expression in the intestine. Inflammatory response mediated by increased NF-κB activation and ICAM-1 expression may play an important role in the pathogenesis of acute gut mucosal injury following TBI. 展开更多
关键词 Traumatic brain injury INTESTINE nuclear factor kappa b Intercellular adhesion molecule-1 Inflammatory response
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Effects of L-3-n-butylphthalide on caspase-3 and nuclear factor kappa-B expression in primary basal forebrain and hippocampal cultures after beta-amyloid peptide 1-42 treatment 被引量:3
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作者 Ruixia Wang Yong Zhang +12 位作者 Liangliang Jiang Guozhao Ma Qingxi Fu Jialong Li Peng Yan Lunqian Shen Yabo Feng Chunxia Li Zaiying Pang Yuanxiao Cui Chunfu Chen Yifeng Du Zhaokong Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2009年第4期252-257,共6页
BACKGROUND: L-3-n-butylphthalide (L-NBP) can inhibit phosphorylation of tau protein and reduce the neurotoxicity of beta-amyloid peptide 1-42 (Aβ1-42). OBJECTIVE: To observe the neuroprotective effects of L-NBP... BACKGROUND: L-3-n-butylphthalide (L-NBP) can inhibit phosphorylation of tau protein and reduce the neurotoxicity of beta-amyloid peptide 1-42 (Aβ1-42). OBJECTIVE: To observe the neuroprotective effects of L-NBP on caspase-3 and nuclear factor kappa-B (NF- K B) expression in a rat model of Alzheimer's disease. DESIGN, TIME AND SETTING: A cell experiment was performed at the Central Laboratory of Provincial Hospital affiliated to Shandong University between January 2008 and August 2008. MATERIALS: L-NBP (purity 〉 98%) was provided by Shijiazhuang Pharma Group NBP Pharmaceutical Company Limited. Aβ1-42, 3-[4,5-dimethylthiazolo-2]-2,5 iphenyltetrazolium bromide (MTT), and rabbit anti-Caspase-3 polyclonal antibody were provided by Cell Signaling, USA; goat anti-choactase and rabbit anti-NF- kB antibodies were provided by Santa Cruz, USA. METHODS: Primary cultures were generated from rat basal forebrain and hippocampal neurons at 17 or 19 days of gestation. The cells were assigned into five groups: the control group, the Aβ1-42 group (2 μmol/L), the Aβ1-42 + 0.1 μmol/L L-NBP group, the Aβ1-42 + 1 μ mol/L L-NBP group, and the Aβ1-42 + 10μmol/L L-NBP group. The neurons were treated with Aβ1-42 (2 μmol/L) alone or in combination with L-NBP (0.1, 1, 10 μmol/L) for 48 hours. Cells in the control group were incubated in PBS. MAIN OUTCOME MEASURES: Morphologic changes were evaluated using inverted microscopy, viability using the M-I-I- method, and the changes in caspase-3 and NF- k B expression using Western blot. RESULTS: Induction with Aβ1-42 for 48 hours caused cell death and soma atrophy, and increased caspase-3 and NF- K B expression (P 〈 0.05). L-NBP blocked these changes in cell morphology, decreased caspase-3 and NF- k B expression (P 〈 0.05), and improved cell viability, especially at the high dose (P 〈 0.05). CONCLUSION: AI3^-42 is toxic to basal forebrain and hippocampal primary neurons; L-NBP protects against this toxicity and inhibits the induction of caspase-3 and NF- K B expression. 展开更多
关键词 L-3-n-butylphthalide cholinergic neurons beta-amyloid peptide 1-42 CASPASE-3 nuclear factor kappa-b
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Inhibition of p38 mitogen-activated protein kinase attenuates experimental autoimmune hepatitis: Involvement of nuclear factor kappa B 被引量:7
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作者 Xiong Ma Yi-Tao Jia De-Kai Qiu 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第31期4249-4254,共6页
To investigate the role of p38 mitogen-activated protein kinase (p38MAPK) in murine experimental autoimmune hepatitis (EAH).METHODS: To induce EAH, the syngeneic S-100 antigen emulsified in complete Freud's adju... To investigate the role of p38 mitogen-activated protein kinase (p38MAPK) in murine experimental autoimmune hepatitis (EAH).METHODS: To induce EAH, the syngeneic S-100 antigen emulsified in complete Freud's adjuvant was injected intraperitoneally into adult male C57BI/6 mice. Liver injury was assessed by serum ALT and liver histology. The expression and activity of p38 MAPK were measured by Western blot and kinase activity assays. In addition, DNA binding activities of nuclear factor kappa B (NF-KB) were analyzed by electrophoretic mobility shift assay. The effects of SB203580, a specific p38 MAPK inhibitor, on liver injuries and expression of proinflammatory cytokines (interferon-y, IL-12, IL-1β and TNF-α) were observed.RESULTS: The activity of p38 MAPK and NF-~:B was increased and reached its peak 14 or 21 d after the first syngeneic S-100 administration. Inhibition of p38 MAPK activation by SB203580 decreased the activation of NF-~:B and the expression of proinflammatory cytokines. Moreover, hepatic injuries were improved significantly after SB203580 administration. 展开更多
关键词 Autoimmune hepatitis p38 mitogen-activatedprotein kinase nuclear factor kappa b Proinflammatorycytokines
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BMS-345541 inhibited nuclear factor kappa B expression and improved locomotor function recovery in rats after acute spinal cord injury 被引量:1
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作者 Xin Han Shouyu Wang Zhen Zhang Decheng Lu Hairun Liu 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第23期1775-1779,共5页
This study sought to elucidate the changes of nuclear factor kappa B (NF-KB) expression and locomotor function of hind limb after subdural injection of BMS-345541 was applied in rats with acute spinal cord injury. T... This study sought to elucidate the changes of nuclear factor kappa B (NF-KB) expression and locomotor function of hind limb after subdural injection of BMS-345541 was applied in rats with acute spinal cord injury. The results indicated that BMS-345541 treatment reduced the expression of NF-kB at 24 hours after injury, compared with normal saline-treated rats. This treatment also led to a significant improvement in locomotor functional recovery at 14 days after injury. Overall, the findings demonstrated that BMS-345541 significantly ameliorated spinal cord injury-induced hind limb dysfunction by inhibiting the expression of NF-kB after spinal cord injury. 展开更多
关键词 spinal cord injury bMS-345541 nuclear factor kappa b locomotor function neural regeneration
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Effect of Helicobacter pylori cdrA on interleukin-8 secretions and nuclear factor kappa B activation 被引量:3
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作者 Hiroaki Takeuchi Ya-Nan Zhang +5 位作者 Dawn A Israel Richard M Peek Jr Mikio Kamioka Hideo Yanai Norihito Morimoto Tetsuro Sugiura 《World Journal of Gastroenterology》 SCIE CAS CSCD 2012年第5期425-434,共10页
AIM: To investigate genetic diversity of Helicobacter pylori (H. pylorl) cell division-related gene A (cdrA) and its effect on the host response.METHODS: Inactivation of H. py/ori cdrA, which is involved in ceil... AIM: To investigate genetic diversity of Helicobacter pylori (H. pylorl) cell division-related gene A (cdrA) and its effect on the host response.METHODS: Inactivation of H. py/ori cdrA, which is involved in ceil division and morphological elonga- tion, has a role in chronic persistent infections. Ge- netic property of H. pylori cdrA was evaluated using polymerase chain reaction and sequencing in 128 (77 American and 51 Japanese) clinical isolates obtained from 48 and 51 patients, respectively. Enzyme-linked immunosorbent assay was performed to measure in- terleukin-8 (IL-8) secretion with gastric biopsy speci- mens obtained from American patients colonized with cdrA-positive or -negative strains and AGS cells co- cultured with wild-type HPK5 (cdrA-positive) or its de- rivative HPKT510 (cdrA-disruptant). Furthermore, the cytotoxin-associated gene A (cagA) status (transloca- tion and phosphorylation) and kinetics of transcription factors [nuclear factor-kappa B (NF-~:B) and inhibition kappa B] were investigated in AGS cells co-cultured with HPK5, HPKT510 and its derivative HPKSCA (cagA- disruptant) by western blotting analysis with immuno- precipitation. RESULTS: Genetic diversity of the H. pylori cdrA gene demonstrated that the cdrA status segregated into two categories including four allele types, cdrA-positive (al- lele types, I and 11 ) and cdrA-negative (allele types; 111 and IV) categories, respectively. Almost all Japanese isolates were cdrA-positive ( 1 : 7.8% and 11 : 90.2%), whereas 16.9% of American isolates were cdrA-positive (11) and 83.1% were cdrA-negative (nl: 37.7% and IV: 45.5%), indicating extended diversity of cdrA in individual American isolates. Comparison of each isolate from different regions (antrum and corpus) in the stomach of 29 Americans revealed that cdrA status was identical in both isolates from different regions in 17 cases. However, 12 cases had a different cdrA al- lele and 6 of them exhibited a different cdrA category between two regions in the stomach. Furthermore, in 5 of the 6 cases possessing a different cdrA category, cdrA-negative isolate existed in the corpus, suggesting that cdrA-negative strain is more adaptable to coloni- zation in the corpus. IL-8 secretions from AGS revealed that IL-8 levels induced by a cdrA-disrupted HPKT510 was significantly lower (P 〈 0.01) compared to wild- type HPK5: corresponding to 50%-60% of those of wild-type HPK5. These data coincided with in vivo data that an average value of IL-8 in biopsy specimens from cdrA-positive and cdrA-negative groups was 215.6 and 135.9 pg/mL, respectively. Western blotting analysis documented that HPKT510 had no effect on CagA translocation and phosphorylation, however, nuclear accumulation of NF-κB was lower by HPKT510 com- pared to HPK5. CONCLUSION: Colonization by a cdrA-negative or cdrA-dysfunctional strain resulted in decreased IL-8 production and repression of NF-κB, and hence, atten- uate the host immunity leading to persistent infection. 展开更多
关键词 Helicobacter pylori cell division-relatedgene A Genetic diversity Host immune response Interleukin-8 secretion nuclear factor kappa .b Persis-tent infection
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Inhibitory effects of Shuanghuanglian injection on nuclear factor-kappa B expression in mice with viral encephalitis in a time-and dose-dependent manner 被引量:1
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作者 Ye Tian Caiping Han Naibing Gu Zhengli Di Gejuan Zhang Hui Lei 《Neural Regeneration Research》 SCIE CAS CSCD 2011年第24期1865-1869,共5页
Previous studies have confirmed that the anti-virus effects of Shuanghuanglian injection may be associated with nuclear factor-kappa B activity. This study observed nuclear factor-kappa B expression in mice with viral... Previous studies have confirmed that the anti-virus effects of Shuanghuanglian injection may be associated with nuclear factor-kappa B activity. This study observed nuclear factor-kappa B expression in mice with viral encephalitis, and showed significant decreases in nuclear factor-kappa B protein and mRNA levels following Shuanghuanglian injection. The inhibitory effect was more significant with prolonged intervention duration and increased treatment dose. These findings verify that Shuanghuanglian injection plays a therapeutic role in viral encephalitis by reducing expression of nuclear factor-kappa B in a time- and dose-dependent manner. 展开更多
关键词 nuclear factor-kappa b viral encephalitis MICE gene expression Shuanghuanglian injection neural regeneration
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Shuanghuanglian injection downregulates nuclear factor-kappa B expression in mice with viral encephalitis 被引量:7
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作者 Naibing Gu Ye Tian +3 位作者 Zhengli Di Caiping Han Hui Lei Gejuan Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2012年第33期2592-2599,共8页
A mouse model of viral encephalitis was induced by intracranial injection of a Coxsackie virus B3 suspension. Quantitative real-time reverse transcription-PCR and western blot assay were applied to detect mRNA and pro... A mouse model of viral encephalitis was induced by intracranial injection of a Coxsackie virus B3 suspension. Quantitative real-time reverse transcription-PCR and western blot assay were applied to detect mRNA and protein expression of intelectin-2 and nuclear factor-kappa B in the viral encephalitis and control groups. Nuclear factor-kappa B and intelectin-2 mRNA and protein expression were significantly increased in mice with viral encephalitis. After intraperitoneal injection of Shuanghuanglian at a dose of 1.5 mg/kg for 5 successive days, intelectin-2 and nuclear factor-kappa B protein and mRNA expression were significantly decreased. To elucidate the relationship between intelectin-2 and nuclear factor-kappa B, mice with viral encephalitis were administered an intracerebral injection of 107 pfu recombinant lentivirus expressing intelectin shRNA. Both protein and mRNA levels of intelectin and nuclear factor-kappa B in brain tissue of mice were significantly decreased. Experimental findings suggest that Shuanghuanglian injection may downregulate nuclear factor-kappa B production via suppression of intelectin production, thus inhibiting inflammation associated with viral encephalitis. 展开更多
关键词 intelectin nuclear factor-kappa b viral encephalitis short hairpin RNA Shuanghuanglian injection mice lentivirus nervous system disease traditional Chinese medicine neural regeneration
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Increased Expression and Activity of MMP-9 in C-reactive Protein-induced Human THP-1 Mononuclear Cells Is Related to Activation of Nuclear Factor Kappa-B 被引量:1
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作者 盛富强 程龙献 +1 位作者 曾秋棠 高文 《Journal of Huazhong University of Science and Technology(Medical Sciences)》 SCIE CAS 2009年第4期399-403,共5页
The relation between the expression and activity of MMP-9 in C-reactive protein (CRP)-induced human THP-1 mononuclear cells and the activation of nuclear factor kappa-B (NF-κB) was studied to investigate the poss... The relation between the expression and activity of MMP-9 in C-reactive protein (CRP)-induced human THP-1 mononuclear cells and the activation of nuclear factor kappa-B (NF-κB) was studied to investigate the possible role of CRP in plaque destabilization. Human THP-1 cells were incubated in the presence of CRP at 0 (control group), 25, 50 and 100 μg/mL (CRP groups) for 24 h. In PDTC (a specific NF-κB inhibitor) group, the cells were pre-treated with PDTC at 10 μmol/L and then with 100 μg/mL CRP. The conditioned media (CM) and human THP-1 cells in different groups were harvested. MMP-9 expression in CM and human THP-1 cells was measured by ELISA and Western blotting. MMP-9 activity was assessed by fluorogenic substrates. The expression of NF-κB inhibitor α (IκB-α) and NF-κB p65 was detected by Western blotting and ELISA respectively. The results showed that CRP increased the expression and activity of MMP-9 in a dose-dependent manner in the human THP-1 cells. Western blotting revealed that IiB-α expression was decreased in the cells with the concentrations of CRP and ELISA demonstrated that NF-κB p65 expression in the CRP-induced cells was increased. After pre-treatment of the cells with PDTC at 10 μmol/L, the decrease in IκB-α expression and the increase in NF-κB p65 expression in the CRP-induced cells were inhibited, and the expression and activity of MMP-9 were lowered too. It is concluded that increased expression and activity of MMP-9 in CRP-induced human THP-1 cells may be associated with activation of NF-κB. Down-regulation of the expression and activity of MMP-9 may be a new treatment alternative for plaque stabilization by inhibiting the NF-κB activation. 展开更多
关键词 C-reactive protein human THP-1 mononuclear cell matrix metalloproteinase-9 nuclear factor kappa-b
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Isoflavone Attenuates the Nuclear Transcription Factor Kappa B (NF-<i>κ</i>B) Activation on MPP<sup>+</sup>-Induced Apoptosis of PC12 Cells 被引量:1
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作者 Weidong Cheng Anqi Huang +5 位作者 Li Zhang Depeng Feng Xiaoqian Sun Hengyi Xu Qianru Sun Xueli Li 《Journal of Behavioral and Brain Science》 2020年第5期191-199,共9页
Objective: To explore the underlying molecular mechanisms of cellular response to the challenge by 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis of PC12 cells, an in vitro cell model for Parkinson’s disease, a... Objective: To explore the underlying molecular mechanisms of cellular response to the challenge by 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis of PC12 cells, an in vitro cell model for Parkinson’s disease, and the effect of NF-κB activation on the protection of Parkinson’s disease by Isoflavone (I). Methods: PC12 cells were used to establish the cell model of Parkinson’s disease, and are divided into five groups: control group;MPP+ group;I (Isoflavone) + MPP+ group;I group;SN-50 + MPP+ group. The content of NF-κB in PC12 cells was determined by immunocytochemistry;The viability of PC12 cells after treated with cell-permeable NF-κB inhibitor SN-50 and cell viability were measured by MTT assay;the expression levels of NF-κB p65 in cytoplasm and nuclear fractions were evaluated by western blot analysis;the mRNA expression of NF-κB p65 was analyzed by in situ hybridization (ISH). Results: Compared with the control group, the protein of NF-κB p65 both in cytoplasm and in nuclei was significantly higher than in I + MPP+ and MPP+ groups;similarly, the mRNA expression level of NF-κB p65 gene was also significantly higher;moreover, the protein expression of NF-κB p65 was much lower in I group (P + group, the protein of NF-κB p65 was significantly lower in I + MPP+ group, the mRNA expression level of NF-κB p65 gene was also significantly lower, and the protein expression level of NF-κB p65 was much lower in I + MPP+ group (P + group (P > 0.05). Conclusion: NF-κB activation is essential to MPP+-induced apoptosis in PC12 cells;but Isoflavone can inhibit the cell damage to some extent to execute its protective function, which may be involved in nigral neurodegeneration in patients with Parkinson’s disease. 展开更多
关键词 ISOFLAVONE PC12 Cell MPP+ Apoptosis NF-κb p65 nuclear Transcription factor kappa b Parkinson’s Disease
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茯苓甘草合剂辅助西药对慢性阻塞性肺疾病合并肌肉衰减患者NF-κB信号通路的影响 被引量:1
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作者 梁晔 庄洁 +1 位作者 房晓华 张积友 《河北医药》 CAS 2024年第2期196-200,共5页
目的探讨茯苓甘草合剂辅助西药对慢性阻塞性肺疾病(COPD)合并肌肉衰减NF-κB信号通路的影响及分子机制。方法选取2020年8月至2022年8月COPD合并肌肉衰减患者104例,作为研究对象随机数字表法分为对照组和观察组,每组52例。对照组给予西... 目的探讨茯苓甘草合剂辅助西药对慢性阻塞性肺疾病(COPD)合并肌肉衰减NF-κB信号通路的影响及分子机制。方法选取2020年8月至2022年8月COPD合并肌肉衰减患者104例,作为研究对象随机数字表法分为对照组和观察组,每组52例。对照组给予西药治疗,观察组给予西药+茯苓甘草合剂治疗。统计2组中医疗效、不良反应及治疗前后中医证候积分、NF-κB mRNA、蛋白及因子[白细胞介素-8(IL-8)、白细胞介素-1(IL-1)、肿瘤坏死因子-α(TNF-α)]、营养状况指标[转铁蛋白(Tf)、血红蛋白(Hb)、白蛋白(ALB)]、肌肉衰减相关指标[握力试验、起立-行走计时测试(TUGT)、5次坐立试验(FTSST)、肌少症筛查问卷(SARC-F)]。结果观察组中医治疗总有效率[86.54%(45/52)]高于对照组[67.31%(35/52)](P<0.05);治疗1个月、3个月后观察组中医证候积分低于对照组(P<0.05);治疗1个月、3个月后观察组NF-κB mRNA、NF-κB蛋白、IL-8、IL-1、TNF-α低于对照组(P<0.05);治疗3个月后观察组握力高于对照组,FTSST、TUGT、SARC-F评分低于对照组(P<0.05);治疗期间,2组均未出现明显不良反应。结论茯苓甘草合剂辅助西药治疗COPD合并肌肉衰减效果确切,可通过抑制NF-κB信号通路,减轻炎性反应,改善患者营养状态,有效改善临床症状,且安全性高。 展开更多
关键词 茯苓甘草合剂 肺疾病 慢性阻塞性 肌肉衰减 NF-Κb信号通路 中医证候
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BRD4/NF-κB信号通路介导的铁死亡参与三阴性乳腺癌化疗耐药的机制
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作者 张硕稳 李丹 +2 位作者 贺静 杜志兴 裴永彬 《重庆医科大学学报》 CAS CSCD 北大核心 2024年第7期844-852,共9页
目的:探讨溴域蛋白亚家族4(bromodomain protein subfamily 4,BRD4)/核因子κB(nuclear factor kappa-B,NF-κB)信号通路介导的铁死亡参与乳腺癌恶性生物学行为的机制。方法:多柔比星(Doxorubicin,DOX)抗性MDA-MB-231细胞(MDAMB-231/DOX... 目的:探讨溴域蛋白亚家族4(bromodomain protein subfamily 4,BRD4)/核因子κB(nuclear factor kappa-B,NF-κB)信号通路介导的铁死亡参与乳腺癌恶性生物学行为的机制。方法:多柔比星(Doxorubicin,DOX)抗性MDA-MB-231细胞(MDAMB-231/DOX)分为对照(Con)组、DOX组和si-BRD4+DOX组。si-BRD4+DOX组在用si-BRD4转染MDA-MB-231/DOX细胞48 h后,用1μmol/L DOX处理细胞24 h。通过集落形成试验和5-乙炔基-2′-脱氧尿苷(5-Ethynyl-2′-deoxyuridine,EdU)分析评估细胞增殖能力。通过FerroOrange、liperfloo检测细胞亚铁离子浓度和脂质过氧化水平。将15只雌性BALB/c-nu小鼠随机分为3组:对照组、DOX组、DOX+si-BRD4组,每组5只,用于建立MDA-MB-231/DOX细胞皮下接种模型。通过qRT-PCR、蛋白质印迹、免疫组化分析BRD4/NF-κB信号通路表达。结果:与si-NC组相比,si-BRD4#1和si-BRD4#2组MDA-MB-231、BT549细胞的细胞克隆数、EDU阳性染色、谷胱甘肽(glutathione,GSH)水平均降低(P<0.001),和MDA-MB-231、BT549细胞亚铁离子水平、活性氧(reactive oxygen species,ROS)水平、氧化型谷胱甘肽(Oxidized glutathione,GSSG)/GSH比值升高(P<0.01)。与亲代细胞(MDA-MB-231)相比,在MDA-MB-231/DOX中BRD4的mRNA和蛋白质表达水平升高。与Con组相比,DOX组细胞中IKβ-α、NF-κB、BRD4表达和ROS水平增加(P<0.05),和细胞克隆数和EDU阳性染色均降低(P<0.05);与DOX组相比,si-BRD4+DOX组细胞中核因子κB抑制蛋白α(Anti-IKB alpha,IKβ-α)、NF-κB表达、细胞克隆数、EDU阳性染色降低(P<0.05),ROS水平升高(P<0.05)。与对照组相比,DOX组肿瘤重量和体积均减少(P<0.05),并且肿瘤组织中TUNEL染色细胞增加(P<0.05)。此外,BRD4+DOX组肿瘤重量和体积较DOX组进一步降低(P<0.001),TUNEL染色细胞进一步增加(P<0.001)。BRD4+DOX组肿瘤组织中Ki-67、BRD4、NF-κB较DOX组下调(P<0.01),4-羟基壬烯醛(4-Hydroxynonenal,4-HNE)上调(P<0.01)。结论:BRD4是一个重要的耐药因子,它可以通过促进NF-κB信号通路的激活来抑制乳腺癌化疗诱导的铁死亡。 展开更多
关键词 溴域蛋白亚家族4 核因子Κb 铁死亡 乳腺癌
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SIRT1/NF-κB信号通路与脑梗死后认知障碍风险及认知障碍程度的相关性分析
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作者 雷延成 张品元 +2 位作者 樊青俐 王进鹏 张豪 《中国现代医学杂志》 CAS 2024年第20期13-18,共6页
目的探讨沉默信息调节因子2相关酶1(SIRT1)/核因子-κB(NF-κB)信号通路与脑梗死后认知障碍风险及认知障碍程度的相关性。方法选取2020年6月—2023年1月青海省人民医院收治的153例急性脑梗死患者,采用简易智力状态检查量表(MMSE)评估患... 目的探讨沉默信息调节因子2相关酶1(SIRT1)/核因子-κB(NF-κB)信号通路与脑梗死后认知障碍风险及认知障碍程度的相关性。方法选取2020年6月—2023年1月青海省人民医院收治的153例急性脑梗死患者,采用简易智力状态检查量表(MMSE)评估患者的认知功能,MMSE评分27~30分的患者作为认知正常组(86例)、MMSE评分≤26分的患者作为认知障碍组(67例)。比较两组蒙特利尔认知评估量表(MoCA)评分及MMSE评分;检测患者SIRT1、NF-κB mRNA相对表达量;采用Pearson法分析SIRT1、NF-κB mRNA相对表达量与MoCA评分和MMSE评分的相关性;绘制受试者工作特征(ROC)曲线,分析SIRT1、NF-κB mRNA相对表达量预测认知功能障碍的价值。结果认知障碍组MMSE评分各项目得分及总分均低于认知正常组(P<0.05)。认知障碍组MoCA评分各项目得分及总分均低于认知正常组(P<0.05)。认知障碍组SIRT1 mRNA相对表达量低于认知正常组,NF-κB mRNA相对表达量高于认知正常组(P<0.05)。重度认知功能障碍患者SIRT1 mRNA相对表达量低于中度和轻度认知功能障碍患者(P<0.05),中度认知功能障碍患者低于轻度认知功能障碍患者(P<0.05),重度认知功能障碍患者NF-κB mRNA相对表达量高于中度和轻度认知功能障碍患者(P<0.05),中度认知功能障碍患者高于轻度认知功能障碍患者(P<0.05)。SIRT1 mRNA相对表达量与MoCA评分和MMSE评分呈正相关(r=0.497和0.532,均P<0.05),NF-κB mRNA相对表达量与MoCA评分和MMSE评分呈负相关(r=-0.518和-0.552,均P<0.05)。ROC曲线结果显示,SIRT1、NF-κB mRNA相对表达量单独及联合预测急性脑梗死认知功能障碍发生的曲线下面积分别为0.825(95%CI:0.749,0.901)、0.897(95%CI:0.826,0.968)、0.948(95%CI:0.916,0.980),敏感性分别为73.1%(95%CI:0.674,0.852)、83.6%(95%CI:0.788,0.949)、88.1%(95%CI:0.835,0.918),特异性分别为75.6%(95%CI:0.648,0.842)、80.2%(95%CI:0.755,0.916)、84.9%(95%CI:0.806,0.882)。结论急性脑梗死后认知功能障碍患者SIRT1 mRNA相对表达量较低,NF-κB mRNA相对表达量较高,且表达量与认知功能障碍程度具有关,通过检测其表达可为预测急性脑梗死后认知功能障碍的发生提供帮助。 展开更多
关键词 脑梗死 认知功能障碍 沉默信息调节因子2相关酶1 核因子-Κb 相关性
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颗粒蛋白前体对脓毒症急性肺损伤小鼠肺组织核转录因子-κB的表达的影响
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作者 彭乔治 徐昉 林时辉 《重庆医科大学学报》 CAS CSCD 北大核心 2024年第4期395-400,共6页
目的:探讨颗粒蛋白前体(progranulin,PGRN)对脓毒症急性肺损伤(acute lung injury,ALI)的影响及可能机制。方法:将C57BL/6小鼠随机分为对照组(Control组)、急性肺损伤组(CLP组)、颗粒蛋白前体治疗组(CLP+PGRN组)。采用盲肠结扎穿刺术(ce... 目的:探讨颗粒蛋白前体(progranulin,PGRN)对脓毒症急性肺损伤(acute lung injury,ALI)的影响及可能机制。方法:将C57BL/6小鼠随机分为对照组(Control组)、急性肺损伤组(CLP组)、颗粒蛋白前体治疗组(CLP+PGRN组)。采用盲肠结扎穿刺术(cecal ligation and puncture,CLP)构建小鼠脓毒症ALI模型,CLP+PGRN组在CLP处理半小时后使用PGRN腹腔注射。24 h后麻醉并处死小鼠,取小鼠肺HE染色观察肺组织病理损伤;TUNEL法检测肺部细胞凋亡情况;免疫荧光染色检测肺组织中核转录因子-κB(nuclear factor kappa B,NF-κB)水平;Western blot法检测NF-κB、总p65和磷酸化p65表达水平;RT-qPCR检测NF-κB和炎症细胞因子水平。结果:和Control组相比,CLP组和CLP+PGRN组肺损伤加重,促炎细胞因子升高,肺组织中细胞凋亡增加,NF-κB、p65和p-p65的表达水平明显增加;与CLP组相比,CLP+PGRN组肺组织损伤和凋亡减轻,促炎细胞因子降低,抑炎细胞因子升高,NF-κB、p65和p-p65的表达明显减少。结论:PGRN可以减轻脓毒症小鼠急性肺损伤,其机制可能与抑制NF-κB、p65表达和p65磷酸化有关。 展开更多
关键词 急性肺损伤 颗粒蛋白前体 组织核转录因子-κb P65
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脂氧素A4抑制TLR4/MyD88/NF-κB通路减缓脓毒症性急性肾损伤
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作者 龚书豪 曹春水 +1 位作者 王缨 梅松波 《安徽医科大学学报》 CAS 北大核心 2024年第2期275-281,共7页
目的探讨脂氧素A4(LXA4)通过抑制TLR4/MyD88/NF-κB通路减缓脓毒症性急性肾损伤(SAKI)。方法将40只无特定病原体级雄性C57BL/6J小鼠随机分为SAKI组、SAKI+LXA4组、假手术组、假手术+LXA4组,每组10只。采用盲肠结扎穿孔术进行SAKI造模,SA... 目的探讨脂氧素A4(LXA4)通过抑制TLR4/MyD88/NF-κB通路减缓脓毒症性急性肾损伤(SAKI)。方法将40只无特定病原体级雄性C57BL/6J小鼠随机分为SAKI组、SAKI+LXA4组、假手术组、假手术+LXA4组,每组10只。采用盲肠结扎穿孔术进行SAKI造模,SAKI+LXA4组、假手术+LXA4组在术后30 min腹腔注射LXA4(40 ng/kg)。各组小鼠在造模术后24 h收集血清、尿液、肾组织。酶联免疫吸附试验(ELISA)测定各组小鼠血肌酐(Scr)、血尿素氮(Bun)、白细胞介素-1β(IL-1β)、IL-6、肿瘤坏死因子-α(TNF-α),尿液中性粒细胞明胶酶相关性脂质运载蛋白(NGAL)及肾损伤分子1(KIM-1);HE及PAS染色观察小鼠肾脏损伤情况;实时荧光定量PCR检测各组小鼠肾脏Toll样受体4(TLR4)、髓样分化因子88(MyD88)、核因子-κB p65(NF-κB p65)mRNA水平;免疫组化法、蛋白免疫印迹实验检测各组小鼠TLR4、MyD88、NF-κB p65、磷酸化NF-κB p65(p-NF-κB p65)的表达。结果ELISA实验提示SAKI组Scr、Bun、IL-1β、IL-6、TNF-α、NGAL、KIM-1水平均高于SAKI+LXA4组(P<0.05),假手术组及假手术+LXA4组Scr、Bun、IL-1β、IL-6、TNF-α、NGAL、KIM-1无明显上升;HE及PAS染色提示SAKI组肾损伤程度明显高于SAKI+LXA4组(P<0.05),假手术组及假手术+LXA4组无明显肾损伤;实时荧光定量PCR提示SAKI组较SAKI+LXA4组TLR4、MyD88、NF-κB p65 mRNA升高(P<0.05),假手术组与假手术+LXA4组TLR4、MyD88、NF-κB p65 mRNA均低于SAKI组及SAKI+LXA4组(P<0.05);免疫组化法、蛋白免疫印迹实验结果提示SAKI组较SAKI+LXA4组TLR4、MyD88、NF-κB p65、p-NF-κB p65表达升高(P<0.05),假手术组与假手术+LXA4组TLR4、MyD88、NF-κB p65、p-NF-κB p65表达均低于SAKI组及SAKI+LXA4组(P<0.05)。结论TLR4/MyD88/NF-κB通路在SAKI发生发展中起重要作用,LXA4可能通过抑制TLR4/MyD88/NF-κB信号通路减缓SAKI。 展开更多
关键词 脂氧素A4 TOLL样受体4 髓样分化因子88 核转录因子kappa b 脓毒症 急性肾损伤
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