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A rough Brucella mutant induced macrophage death depends on secretion activity of T4SS, but not on cellular txnip- and Caspase-2-mediated signaling pathway

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VETERINARY MICROBIOLOGY 2020年 244卷 108648-108648页

作者： Tian, Mingxing Yin, Yi Lian, Zhengmin Li, Zichen Song, Meiying Hu, Hai Guan, Xiang Ding, Chan Wang, Shaohui Li, Tao Qi, Jingjing Yu, Shengqing Chinese Acad Agr Sci CAAS Shanghai Vet Res Inst Shanghai 200241 Peoples R China Jiangsu Coinnovat Ctr Prevent & Control Important Yangzhou 225009 Jiangsu Peoples R China

Brucella is a facultative intracellular bacterium, dividing into smooth- and rough-type Brucella. Smooth-type Brucella can dissociate into rough mutants with cytotoxicity for macrophages during infection, which is critical for Brucella egress and dissemination. However, the mechanism of cytotoxicity infected by rough Brucella is incomplete. In this study, we verified that a rough-type Brucella (RB14 strain) was cytotoxic for macrophages dependent on Type IV secretion system (T4SS). Two specific T4SS VirB4 and VirB11 mutants were constructed, which affect the secretion of T4SS effectors, but not the expression of T4SS components. Cytotoxicity analysis showed that RB14- induced macrophages death depends on T4SS secretion activity. In a further study, 15 reported T4SS effectors were evaluated in inducing macrophage death using over-expression and transfection methods, the results showed that 15 recombinant strains with over-expression of respective effector were not cytotoxicity. In addition, 10 effectors transfected individually, or co-transfected with five effectors barely induced macrophage death, suggesting that all 15 effectors were not associated with macrophage death. Besides, we also evaluated endoplasmic reticulum (ER) stress, txnip- or Caspase-2 roles in RB14-induced macrophages death. The results showed that inhibition of ER stress, Caspase or Caspase-2 activation was not associated with RB14-infected macrophages death. The casp2 and txnip knockout cells also showed death when infected by the RB14 strain. In all, the RB14-induced macrophage death depends on the secretion activity of T4SS, but not on ER stress, txnip- or Caspase-2 signal pathway. This study provides a deep insight for rough Brucella-induced macrophage death, which favors for elucidating Brucella infection lifecycle.

关键词： Rough-type Brucella Macrophage death Type IV secretion system txnip Caspase-2

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HO-1对LPS攻击大鼠肺泡巨噬细胞模型中IRE1α/txnip/NLRP3信号通路的影响

HO-1对LPS攻击大鼠肺泡巨噬细胞模型中IRE1α/TXNIP/NLRP3信号通...

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作者：胡欣欣天津医科大学

学位级别：硕士

目的内毒素急性肺损伤(ALI)会导致细胞器结构和功能紊乱,其中包括内质网应激(ERS)。硫氧还蛋白互作蛋白(txnip)能够激活NLRP3炎症小体,而IRE1α作为ERS引起的未折叠蛋白质反应(UPR)的一条重要途径可以诱导txnip的表达。血红素氧合酶-1(H... 详细信息

目的内毒素急性肺损伤(ALI)会导致细胞器结构和功能紊乱,其中包括内质网应激(ERS)。硫氧还蛋白互作蛋白(txnip)能够激活NLRP3炎症小体,而IRE1α作为ERS引起的未折叠蛋白质反应(UPR)的一条重要途径可以诱导txnip的表达。血红素氧合酶-1(HO-1)对内毒素ALI的内源性保护作用已经为我们前期研究所证实,但HO-1是否通过ERS所致UPR的IRE1α通路,抑制NLRP3炎症小体激活尚未明确。为此,本研究旨在利用LPS攻击大鼠肺泡巨噬细胞模型探究HO-1对IRE1α/txnip/NLRP3信号通路的影响。内容与方法本实验采用10μg/ml LPS建立内毒素攻击大鼠肺泡巨噬细胞模型,通过运用细胞转染的方法沉默NR8383细胞HO-1,旨在从细胞层面阐述HO-1对NLRP3炎症小体产生的抑制作用与ERS之间的相关性,具体研究内容与方法如下: 第一步、利用HO-1诱导剂hemin与HO-1基因沉默手段检测HO-1对细胞活力的影响,同时在RNA与蛋白质水平上观察NLRP3炎症小体、ASC、caspase-1表达情况与细胞因子(IL-1β、IL-18)含量的变化,初步了解HO-1能够抑制炎症小体的生成。与此同时,还利用免疫荧光技术进一步验证HO-1对细胞内NLRP3炎症小体表达的影响。第二步、观察HO-1诱导剂hemin与HO-1基因沉默对txnip表达的影响,并测定txnip沉默对NLRP3炎症小体、ASC、caspase-1表达情况与细胞因子(IL-1β、IL-18)含量变化的影响,进一步说明HO-1抑制NLRP3炎症小体激活的作用与txnip密切相关。第三步、测定LPS及ERS抑制剂TUDCA预处理下细胞的内质网应激相关蛋白(GRP78、p-PERK、p-IRE1α)、txnip、NLRP3炎症小体、炎症相关蛋白(ASC、caspase-1)表达情况与细胞因子(IL-1β、IL-18)含量变化,阐明ERS能够参与txnip/NLRP3炎症小体的激活。第四步、检测HO-1沉默对p-IRE1α与XBP1的表达含量的影响,并应用IRE1的抑制剂4μ8C深入验证IRE1是否参与调节txnip/NLRP3炎症小体的生成。在本次实验中,我们采用MTT法测定细胞活力、RT-q PCR法检测mRNA含量、Western Blot检测炎症与ERS相关蛋白含量,以及用ELISA试剂盒检测细胞因子的浓度。结果在步骤一中,结果提示,HO-1沉默后无论是RT-q PCR、Western Blot结果还是免疫荧光结果均显示HO-1表达显著下调,提示造模成功。与此同时,实验结果反应出LPS能够显著降低NR8383细胞活力,HO-1沉默后会使细胞活力进一步下降,而HO-1诱导剂hemin会抑制LPS所致的细胞活力降低。另外,LPS处理后NLRP3、ASC、caspase-1表达水平与细胞因子(IL-1β、IL-18)含量上调,此时NLRP3炎症小体的平均荧光强度也增加,但HO-1诱导剂hemin会下调LPS导致的上述蛋白与细胞因子的表达,HO-1沉默会使上述蛋白的表达、细胞因子含量及NLRP3炎症小体平均荧光强度进一步上调,这提示HO-1能够抑制细胞炎症反应。在步骤二中,结果提示LPS会导致txnip的蛋白与RNA表达水平明显提高,而HO-1诱导剂hemin会抑制txnip表达。运用siRNA将txnip沉默后,结果提示,此时LPS导致的NLRP3炎症小体、ASC、caspase-1及细胞因子产生受到抑制,同时也降低了hemin对NLRP3炎症小体产生的抑制作用,这提示txnip与HO-1抑制NLRP3炎症小体激活作用相关。在步骤三中,结果表明LPS能够使ERS标志性蛋白(GRP78、p-PERK、p-IRE1α)的表达含量明显提高,但ERS抑制剂TUDCA会显著降低LPS作用下NP8383细胞内txnip、NLRP3和caspase-1的表达水平,同时也会降低细胞内IL-1β和IL-18的浓度,这表明LPS诱导下txnip/NLRP3炎症小体的生成与ERS密切相关。在步骤四中,结果表明HO-1沉默能够显著提高LPS刺激下的p-IRE1α、GRP78与XBP1的表达,但不影响p-PERK的表达,而且hemin会使抑制LPS所致的p-IRE1α、XBP1表达水平升高。LPS刺激细胞后,hemin使细胞内p-IREα、XBP1、txnip及NLRP3表达水平显著下降,若同时应用hemin与IRE1抑制剂4μ8C,txnip与NLRP3炎症小体表达水平反而升高,这说明HO-1可以通过抑制IRE1-XBP1通路,进而抑制NR8383细胞NLRP3炎症小体的激活。结论HO-1可以抑制LPS攻击大鼠肺泡巨噬细胞内txnip/NLRP3炎症

关键词： HO-1 内毒素内质网应激炎症小体 IRE1α txnip

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Calcium Pyrophosphate And Monosodium Urate Activate The NLRP3 Inflammasome Within Bladder Urothelium Via Reactive Oxygen Species And txnip

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RESEARCH AND REPORTS IN UROLOGY 2019年 11卷 319-325页

作者： Harper, Shelby N. Leidig, Patrick D. Hughes, Francis M., Jr. Jin, Huixia Purves, J. Todd Duke Univ Sch Med Durham NC 27710 USA Duke Univ Med Ctr Dept Surg Div Urol POB 3831 Durham NC 27710 USA Duke Univ Dept Pediat Durham NC 27710 USA

Objective: To investigate the in vitro activation of the NLRP3 inflammasome within bladder urothelium by stone-forming components. Further, to describe the contributions of reactive oxygen species (ROS) and thioredoxin-interacting protein (txnip), an important structural component of the inflammasome, to this activation. Methods: Urothelial cells were harvested and incubated overnight. For agonist studies, cells were treated with varying concentrations of calcium pyrophosphate (CPPD) and monosodium urate (MSU). For inhibitor studies, cells were treated with either N-acetylcysteine (NAC) (1 hr) or Verapamil (4 hrs) prior to incubation with either CPPD (62.5 ug/mL) or MSU (1.25 ug/mL) for 24 hrs. Untreated controls were incubated with ATP (1.25 mM) for 1 hr to maximally stimulate NLRP3 inflammasome activity (measured as caspase-1 cleavage of the fluorogenic substrate Ac-YVAD-AFC). Results are reported as a percentage of maximum ATP response. Results: CPPD and MSU activate caspase-1 in urothelial cells in a dose-dependent manner, reaching similar to 50% and similar to 25% of the ATP response, respectively. Pre-treatment with the general ROS scavenger NAC reduces this activation in a dose-dependent manner. Additionally, activation was suppressed through treatment with Verapamil, a known downregulator of txnip expression. Conclusion: The stone components CPPD and MSU activate NLRP3 in an ROS and txnip-dependent manner in bladder urothelium. These findings demonstrate the importance of ROS and txnip, and suggest that targeting either may be a way to decrease stone-dependent NLRP3 inflammation within the bladder.

关键词： stones urothelium inflammation NLRP3 inflammasome txnip ROS

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Metformin protects against intestinal ischemia-reperfusion injury and cell pyroptosis via txnip-NLRP3-GSDMD pathway

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REDOX BIOLOGY 2020年 32卷 101534页

作者： Jia, Yifan Cui, Ruixia Wang, Cong Feng, Yang Li, Zeyu Tong, Yingmu Qu, Kai Liu, Chang Zhang, Jingyao Xi An Jiao Tong Univ Dept Hepatobiliary Surg Affiliated Hosp 1 Xian 710061 Shaanxi Peoples R China Northwest Univ Dept Rehabil Med Affiliated Hosp Xian Hosp 3 Xian 710021 Shaanxi Peoples R China Xi An Jiao Tong Univ Shaanxi Prov Peoples Hosp Affiliated Hosp 3 Dept Gen SurgMed Coll Xian 710068 Shaanxi Peoples R China Xi An Jiao Tong Univ Dept SICU Affiliated Hosp 1 Xian 710061 Shaanxi Peoples R China

Intestinal ischemia-reperfusion (I/R) injury is a life-threatening vascular emergency and has long been a disturbing problem for surgeons. Oxidative stress is considered a vital factor in I/R injury. Metformin has antioxidative properties and protects against I/R injury. The present study aimed to investigate whether Metformin protects against intestinal I/R injury and reveal the protective mechanism of Metformin. I/R injury was induced in mice by temporary superior mesenteric artery occlusion, and Caco-2 cells were subjected to OGD/R to establish an in vitro model. Different doses of Metformin were administered in vivo and in vitro. We found that I/R injury led to intestinal barrier disruption and cell death by examining histopathological results and the intestinal barrier index, including TER, tight junction proteins and serum biomarkers. We confirmed the existence of pyroptosis in intestinal I/R injury. Moreover, we confirmed the role of pyroptosis in intestinal I/R injury by silencing the gasdermin D (GSDMD). Then, we confirmed that Metformin treatment protected barrier function against intestinal I/R injury and reduced oxidative stress and the inflammatory response. Importantly, Metformin reduced pyroptosis-related proteins, including NLRP3, cleaved caspase-1, and the N-terminus of GSDMD. Knocking down the GSDMD could reversed the protective effects of Metformin, which showed pyroptosis was one of the major cell death pathways controlled by Metformin treatment in setting of intestinal I/R injury. We also discovered that Metformin suppressed the expression of txnip and the interaction between txnip and NLRP3. We performed siRNA knockdown and found that the protective effects were abolished, which further confirmed our findings. In conclusion, we believe that Metformin protects against intestinal I/R injury in a txnip-NLRP3-GSDMD-dependent manner.

关键词： Intestinal I/R injury Metformin Pyroptosis txnip

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Higher levels of thioredoxin interacting protein (txnip) in patients with prediabetes compared to obese normoglycemic subjects

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DIABETES & METABOLIC SYNDROME-CLINICAL RESEARCH & REVIEWS 2019年第1期13卷 734-737页

作者： Gateva, Antoaneta T. Assyov, Yavor S. Velikova, Tsvetelina Kamenov, Zdravko A. Univ Hosp Alexandrovska Med Univ Sofia Clin Endocrinol 1 GeorgiSofiiski Str Sofia 1431 Bulgaria Univ Hosp Lozenetz Dept Clin Immunol Sofia Bulgaria

Background: Thioredoxin interacting protein (txnip) is one of the mediators of oxidative stress induced beta-cell glucotoxisity. txnip might play a key role in impaired glucose homeostasis preceding overt T2DM. The aim of the present study was to compare txnip levels between patients with prediabetes and obese normoglycemic controls and to evaluate the link between txnip and metabolic risk factors. Patients and methods: In the present study we included 79 patients with mean age 50.3 +/- 10.6 years, divided into two age and BMI matched groups -control group with obesity without glycemic disturbances (NGT) (n = 40) and prediabetes (n = 39). Results: We found significantly higher levels of txnip in patients with prediabetes compared to normoglycemic obese controls (54.2 +/- 69.9 vs. 23.9 +/- 47.1 pg/ml;p = 0.03). The levels of txnip gradually increased from normal glucose tolerance trough IFG/IGT only to IFG + IGT (27,1;44.0;49.9 and 95.7 pg/ml respectively;p = 0.025 between NGT and IFG + IGT). txnip levels correlated weakly only with fasting blood glucose (r = 0.235;p = 0.04) but not with glucose during OGTT or the markers of insulin resistance. Conclusions: The levels of txnip are higher in patients with prediabetes compared to normoglycemic controls as they increase gradually from NGT trough IFG/IGT only to IFG + IGT. (c) 2018 Diabetes India. Published by Elsevier Ltd. All rights reserved.

关键词： txnip Prediabetes Glucotoxicity

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Dimethyl fumarate ameliorates diabetes-associated vascular complications through ROS-txnip-NLRP3 inflammasome pathway

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LIFE SCIENCES 2020年第0期256卷 117887-117887页

作者： Amin, Fatma M. Abdelaziz, Rania R. Hamed, Mohamed F. Nader, Manar A. Shehatou, George S. G. Mansoura Univ Fac Pharm Dept Pharmacol & Toxicol Mansoura Egypt Mansoura Univ Fac Vet Med Dept Pathol Mansoura Egypt Delta Univ Sci & Technol Fac Pharm Dept Pharmacol & Biochem Gamasa City Egypt

Vascular complications are a leading cause of morbidity and mortality among diabetic patients. This work aimed to investigate possible influences of dimethyl fumarate (DMF) on streptozotocin (STZ) diabetes-associated vascular complications in rats, exploring its potential to modulate ROS-txnip-NLRP3 inflammasome pathway. Two weeks after induction of diabetes (via a single injection of 50 mg/kg STZ, i.p.), diabetic rats were administered either DMF (25 mg/kg/day) or its vehicle for further eight weeks. Age-matched normal and DMF-administered non-diabetic rats served as controls. DMF treatment elicited a mild ameliorative effect on diabetic glycemia. DMF reduced serum TG and AGE levels and enhanced serum HDL-C concentrations in diabetic rats. Moreover, DMF significantly diminished aortic levels of ROS and MDA and restored aortic GSH, SOD and Nrf2 to near-normal levels in STZ rats. Aortic mRNA levels of txnip, NLRP3 and NF-kappa B p65 in diabetic rats were significantly reduced by DMF treatment. Serum and aortic protein levels of txnip and aortic contents of IL-1 beta, iNOS, NLRP3 and TGF-beta 1 were significantly lower in DMF-diabetic animals than non-treated diabetic rats. Furthermore, protein expression of TNF-alpha and caspase-3 in diabetic aortas was greatly attenuated by DMF administration. DMF enhanced eNOS mRNA and protein levels and increased bioavailable NO in diabetic aortas. Functionally, DMF attenuated contractile responses of diabetic aortic rings to KCl and phenylephrine and enhanced their relaxant responses to acetylcholine. DMF also mitigated diabetes-induced fibrous tissue proliferation in aortic tunica media. Collectively, these findings demonstrate that DMF offered vasculoprotective influences on diabetic aortas via attenuation of ROS-txnip-NLRP3 inflammasome pathway.

关键词： Diabetes STZ Aorta Dimethyl fumarate txnip NLRP3 ROS TNF-alpha IL-1 beta Caspase-3 eNOS

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基于txnip/NLRP3信号通路探讨亚麻木酚素改善CIH暴露小鼠心肌损伤的作用及机制

基于TXNIP/NLRP3信号通路探讨亚麻木酚素改善CIH暴露小鼠心肌损伤...

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作者：任静河北中医学院

学位级别：硕士

目的探讨亚麻木酚素(secoisolariciresinol dilucoside,SDG)对慢性间歇性低氧(chronic intermittent hypoxia,CIH)小鼠心肌损伤的影响及机制。方法亚麻木酚素灌胃治疗慢性间歇性低氧小鼠,检测各组小鼠心功能(EF、FS、LVEDV、LVESV)、心... 详细信息

目的探讨亚麻木酚素(secoisolariciresinol dilucoside,SDG)对慢性间歇性低氧(chronic intermittent hypoxia,CIH)小鼠心肌损伤的影响及机制。方法亚麻木酚素灌胃治疗慢性间歇性低氧小鼠,检测各组小鼠心功能(EF、FS、LVEDV、LVESV)、心肌组织HE染色及血清中心肌酶CK、LDH-L浓度,观察SDG对CIH小鼠心肌损伤的影响。检测各组小鼠血清中炎症因子IL-6、IL-1β、TNF-α的含量水平,观察SDG对CIH小鼠心肌炎症的影响。Western blot检测NLRP3、pro-caspase-1、caspase-1、ASC、IL-18和IL-1β蛋白,观察SDG对CIH小鼠心肌组织中NLRP3炎性小体的影响。TBA、NBT法检测CIH小鼠心肌组织匀浆中MDA、SOD水平,观测SDG对CIH小鼠心肌组织中氧化应激程度的影响。免疫组化和Western blot分别检测CIH小鼠心肌组织中txnip蛋白表达情况,观测SDG对CIH小鼠心肌中txnip蛋白的影响。结果CIH暴露后,小鼠出现心功能(EF、FS、LVESV和LVEDV)障碍,心肌组织切片HE染色可见的显著的病理改变如心肌细胞排列紊乱,细胞明显肿胀,细胞间隙增大,同时还有炎症细胞浸润,心肌纤维断裂溶解、坏死,检测到血清中心肌酶指标(LDH-L、CK)浓度显著升高(P<0.01),继而检测到CIH组小鼠心肌组织中NLRP3、pro-caspase-1、caspase-1、ASC、IL-1β和IL-18蛋白表达明显升高,以及检测到心肌组织中MDA含量明显升高(P<0.01),和SOD活性明显降低(P<0.01),最后检测到txnip在免疫组化(P<0.01)和WB(P<0.05)中表达升高。亚麻木酚素治疗后,检测到CIH小鼠心功能(EF、FS、LVEDV、LVESV)恢复以及心肌病理切片可见心肌细胞排列大致整齐,细胞间隙减小,炎症细胞浸润减少;CIH+SDG组小鼠血清中(LDH-L、CK)浓度显著下降(P<0.05),NLRP3、pro-caspase-1、caspase-1、ASC、IL-18和IL-1β蛋白表达明显降低(P<0.05),心肌组织匀浆中MDA含量显著下降(P<0.05),SOD含量明显升高(P<0.01),txnip蛋白免疫组化(P<0.01)和WB(P<0.05)表达下降。结论亚麻木酚素可以通过抗氧化作用调节txnip/NLRP3信号通路改善CIH诱发小鼠的心肌损伤。

关键词：亚麻木酚素慢性间歇性低氧氧化应激心肌损伤 NLRP3炎性小体 txnip

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Nrf2通过调节Trx1/txnip复合物抑制炎症小体活化在干性AMD中的机制研究

Nrf2通过调节Trx1/TXNIP复合物抑制炎症小体活化在干性AMD中的机...

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作者：杨倩安徽医科大学

学位级别：硕士

目的年龄相关性黄斑变性（age-related macular degeneration,AMD）主要发生于50岁以上的中老年,患者双眼相继或者同时发病,最终导致中心视力模糊,视力下降、视物变形等。其中慢性炎症是AMD发病的重要机制。课题组前期研究发现,mi R-27a... 详细信息

目的年龄相关性黄斑变性（age-related macular degeneration,AMD）主要发生于50岁以上的中老年,患者双眼相继或者同时发病,最终导致中心视力模糊,视力下降、视物变形等。其中慢性炎症是AMD发病的重要机制。课题组前期研究发现,mi R-27a在AMD患者的血液中表达上调,并通过RNA数据库发现硫氧还蛋白相互作用蛋白（Thioredoxin interacting protein,txnip）为mi R-27a的下游基因,与硫氧还蛋白（Thioredoxin,Trx1）在细胞中已复合物形式。同时,文献证实核转录因子（NE-E2 related factor 2,Nrf2）在AMD患者中具有抗氧化作用。所以本课题探讨Nrf2调控txnip/Trx1在过氧化氢（hydrogen peroxide,H2O2）诱导的视网膜色素上皮细胞（retinal pigmental epithelium,RPE）氧化损伤模型和C57BL/6小鼠视网膜蓝光LED灯诱导光损伤模型中的信号通路机制,进一步揭示AMD的发病机制,并为临床研究提供新的思路。方法1.氧化应激细胞模型建立:体外培养ARPE-19细胞,用不同浓度H2O2（0μM、100μM、200μM、300μM、400μM、500μM）处理ARPE-19细胞1h,1.5h,2h,采用CCK-8法检测细胞增殖能力,确定H2O2作用浓度和时间;2.H2O2干预后细胞ROS的生成:不同浓度H2O2（0μM、100μM、200μM、300μM、400μM、500μM）处理ARPE-19细胞1h后,采用DCFH-DA荧光探针法检测活性氧（reactive oxygen species,ROS）水平的改变;3.氧化应激状态下txnip的定位和水平改变:100μM H2O2诱导的ARPE-19细胞1h后,采用免疫荧光染色法检测氧化损伤条件下,txnip的定位及水平改变;4.氧化应激状态下ARPE-19细胞功能变化:100μM H2O2诱导的ARPE-19细胞1h后,采用划痕实验,确定txnip对于H2O2诱导的ARPE-19细胞的迁移的影响;5.核转录因子Nrf2、txnip、Trx1对ARPE-19细胞抗氧化应激能力和炎症因子的影响:采用定量即时聚合酶链锁反应（quantitative real time polymerase chain reaction,q-PCR）及免疫印迹法（western blot,WB）测定Nrf2、txnip、Trx1和炎症相关因子及蛋白表达的变化。流式细胞术检测活性氧生成情况;6.小鼠光损伤模型建立:对C57BL/6小鼠行波长460nm,强度3000lux的蓝光LED灯光照2h,于5d后采用HE染色检查视网膜厚度变化、ERG检测视网膜功能状态,评估光损伤小鼠视网膜氧化模型是否建立;7.小鼠光损伤模型对视网膜Nrf2、txnip、Trx1的影响:采用q PCR法和WB法测定小鼠视网膜光损伤条件下,Nrf2、txnip、Trx1 m RNA和蛋白质表达变化;8.光损伤模型下,视网膜功能变化:玻璃体腔注射叔丁基对苯二酚（Tert-butylhydroquinone,t BHQ）激活剂激活Nrf2及慢病毒Trx转染后,蓝光光照2h,5d后行ERG检测的小鼠视网膜功能的变化。9.光损伤模型下,视网膜病理变化:玻璃体腔注射t BHQ激活剂激活Nrf2及慢病毒Trx1转染后,蓝光光照2h,5d后行HE检测的小鼠视网膜病理变化。结果1.氧化应激细胞模型建立:H2O2在100μM浓度干预1h后,细胞活性开始下降,并且随着浓度和作用时间的增加,细胞活性不断下降,300μM干预1h后已超过半数致死量,故选择100μM H2O2干预1h为最适作用浓度和时间建立细胞模型;2.流式结果分析显示:不同浓度的H2O2（0-500μM）干预ARPE-19细胞后,H2O2浓度与ROS生成量在一定范围内成正比关系;3.细胞免疫荧光结果表明:与正常组比较,100μM H2O2干预1h后,胞浆txnip增多,胞核txnip减少;4.细胞迁移实验显示:H2O2处理组较正常组,细胞迁移率降低,而si-Trx1组,细胞迁移率降低更明显;***2、txnip、Trx1对ARPE-19细胞抗氧化应激能力和炎症因子的影响:使用30μM t BHQ激活Nrf2,si-Trx1转染ARPE-19细胞,根据q PCR及WB结果显示,相较于对照组,H2O2处理组的Nrf2和Trx1表达减少,胞浆txnip表达上升,炎症相关因子和蛋白IL-18、IL-1β、caspase1、NLRP3表达上升;与H2O2处理组相比,t BHQ组Nrf2表达增加,txnip、IL-18、IL-1β、caspase1、NLRP

关键词：氧化应激年龄相关性黄斑变性炎症小体 txnip

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TRX-1和txnip在膀胱尿路上皮癌中的表达及其意义

TRX-1和TXNIP在膀胱尿路上皮癌中的表达及其意义

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作者：甘欧大连医科大学

学位级别：硕士

目的:探讨硫氧还蛋白-1（TRX-1）和硫氧还蛋白互作蛋白（txnip）在尿路上皮癌及癌旁组织中的表达及意义。方法:查询2014年1月至2014年12月中,在辽宁省肿瘤医院进行膀胱肿瘤切除,收集病理诊断为膀胱尿路上皮癌的患者33例,其中13例患者的... 详细信息

目的:探讨硫氧还蛋白-1（TRX-1）和硫氧还蛋白互作蛋白（txnip）在尿路上皮癌及癌旁组织中的表达及意义。方法:查询2014年1月至2014年12月中,在辽宁省肿瘤医院进行膀胱肿瘤切除,收集病理诊断为膀胱尿路上皮癌的患者33例,其中13例患者的石蜡标本都收集了癌组织和癌旁组织（大于肿瘤切缘5cm）的病理石蜡,其中20例只收集癌组织石蜡包块。对石蜡包埋处理的组织切片,通过免疫组化SP法,测定膀胱癌组织及癌旁组织中TRX-1及txnip的表达水平。对结果进行统计学分析,阐明TRX-1及txnip在膀胱癌组织中的表达情况,以及TRX-1及txnip的表达与患者临床病理因素之间的关系和二者之间的相关性。结果:1、在33例膀胱癌组织中,TRX-1高表达21例,占比63.6%,低表达12例,占比36.4%。在13例癌周围正常组织中,TRX-1高表达3例,占比23.1%,低表达10例,占比76.9%。TRX-1在膀胱癌中的表达高于癌周组织,差异有统计学意义（χ2=4.630,P=0.031<0.05）。TRX-1主要存在于胞浆内,少数存在于细胞核。2、运用Fisher精确检验检测TRX-1的表达水平与患者的年龄、性别、肿瘤大小、病理分级、是否侵犯肌层、T分级、淋巴结转移和TNM分期的关系。结果发现TRX-1在膀胱癌中的表达与患者年龄、患者性别、肿瘤最大直径、淋巴结是否转移等均无差异（P>0.05）;TRX-1的表达与病理分级、T分级、是否侵犯肌层、TNM分期等均有差异（P<0.005）。3、在膀胱癌组织中,txnip不表达或低表达;在癌旁组织中,txnip高表达,多数存在于细胞质中,少数存在于细胞膜上。txnip在膀胱癌和癌旁组织中的阳性率分别为42.4%和92.3%。txnip在尿路上皮癌中的表达水平低于癌旁组织,差异有统计学意义（χ2=9.443,P<0.05）。4、运用Fisher精确检验检测txnip的表达水平与患者的年龄、性别、肿瘤大小、病理分级、是否侵犯肌层、T分级、淋巴结转移和TNM分期的关系。结果发现txnip在癌组织中的表达情况与患者年龄、患者性别、肿瘤直径、淋巴结是否转移各组的组间均无差异（P>0.05）;txnip的表达与病理分级、T分级、是否侵犯肌层、TNM分期各组的组间均存在显著差异（P<0.05）。5、Spearman相关性分析结果表明,TRX-1在膀胱癌中的表达与txnip的表达存在负相关性（r=﹣0.696,P<0.01）。结论:1、TRX-1在膀胱癌中的表达高于癌旁组织,txnip在膀胱癌中的表达低于癌旁组织。2、TRX-1在膀胱癌中的表达与txnip的表达存在负相关性。3、TRX-1和txnip的表达均与患者年龄、患者性别、肿瘤直径大小,淋巴是否结转移都不存在相关性。TRX-1和txnip与病理分级、T分级、肌层浸润、TNM分期有相关性。TRX-1的表达随着病理分级、T分级、TNM分期的升高而升高;txnip的表达随着病理分级、T分级、TNM分期的升高而降低。以上结果表示,TRX-1和txnip与尿路上皮癌的病理分级,浸润深度等与肿瘤恶性程度相关的指标存在关联,这些指标也都与膀胱癌的浸润发展有关,提示TRX-1和txnip有希望能成为膀胱癌诊断的指标以及评估肿瘤预后的标志物。

关键词：膀胱癌 TRX-1 txnip 免疫组化

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sCD163、txnip与非酒精性脂肪肝的相关性研究

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中文科技期刊数据库（全文版）医药卫生 2021年第7期 265-266页

作者：韩霖昌邑市龙池镇卫生院山东昌邑261300

本研究主要探究?sCD163、txnip与非酒精性脂肪肝的相关性。方法:选择2019年1月-2021年1月就就诊于我院的非酒精性脂肪肝患者45例作为研究组,同期健康体检的患者30例作为观察组,比较两组血清?sCD163、txnip水平,分析其与非酒精性脂肪肝... 详细信息

本研究主要探究?sCD163、txnip与非酒精性脂肪肝的相关性。方法:选择2019年1月-2021年1月就就诊于我院的非酒精性脂肪肝患者45例作为研究组,同期健康体检的患者30例作为观察组,比较两组血清?sCD163、txnip水平,分析其与非酒精性脂肪肝的相关性。结果:研究组中?sCD163、txnip均高于对照组,差异有统计学意义(P<0.05);研究组sCD163与txnip有相关性,呈正相关。结论:血清?sCD163、txnip水平升高是导致非酒精性脂肪肝的重要因素,值得临床关注。

关键词： sCD163 txnip 非酒精性脂肪肝

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