miR-223与胃癌关系的研究进展

消化系统肿瘤是目前最常见的恶性肿瘤之一,其发病率及病死率占全部恶性肿瘤的30%左右,在中国其发病率可占全部恶性肿瘤的50%以上。微小核糖核酸(miRNA)是由21~25个核苷酸组成的非编码RNA,它通过与靶基因的3′端非翻译区(3′-UTR)配对,促进mRNA的降解或抑制mRNA的翻译,从而抑制其靶基因的表达。近年来研究发现,miRNA参与细胞的增殖、分化和凋亡等细胞进程,在包括胃癌在内的多种肿瘤中异常表达。此文就miR-223在胃癌中的研究进展作一综述。     

血清miR-223、IL-6水平与复杂型热性惊厥患儿脑损伤的关系

目的 探讨血清微小核糖核酸-223(miR-223)、白细胞介素-6(IL-6)与复杂型热性惊厥（CFS）患儿脑损伤的关系。方法 选取124例CFS患儿（CFS组）,根据是否发生脑损伤将CFS患儿分为脑损伤组39例和无脑损伤组85例,另选取46名同期健康儿童（对照组）为对照。采用实时荧光定量聚合酶链式反应与酶联免疫吸附法检测血清miR-223与IL-6水平。Spearman相关性法分析血清miR-223、IL-6在CFS患者血清中的相关性,多因素Logistic回归分析影响CFS患儿脑损伤的因素,受试者工作特征曲线分析血清miR-223、IL-6水平对CFS患儿脑损伤的预测价值。结果 与对照组比较,CFS组血清miR-223水平降低,IL-6水平升高（P均<0.05）。CFS患儿血清miR-223与IL-6水平呈负相关（r=-0.800,P<0.05）。124例CFS患儿脑损伤发生率为31.45%(39/124)。全身抽搐、惊厥发作次数≥2次、惊厥发作持续时间≥5 min、IL-6升高为CFS患儿脑损伤的独立危险因素,miR-223升高为独立保护因素（P均<0.05）...     

白细胞介素-6与2型糖尿病及动脉粥样硬化发生发展的关系

白细胞介素（IL）-6是一种多功能的细胞因子,其作为前炎症细胞因子,在炎症反应过程中起着重要的作用。目前糖尿病和动脉粥样硬化被认为是慢性炎症过程,IL-6不但参与了糖尿病及动脉粥样硬化的发生发展,还在一定程度上预示了疾病发生的危险性。本文主要涉及IL-6在糖尿病及动脉粥样硬化发生、发展中的作用及机制研究。     

动脉粥样硬化的炎症信号通路研究进展

<正>动脉粥样硬化(atherosclerosis,AS)是一种慢性炎症疾病,大量人和动物病理生理研究结果支持炎性损伤-反应学说,认为AS病变始于血管内皮细胞(vascular endothelial cells,VEC)受损和由此引起的内皮功能不良[1]。我们从内皮损伤-反应角度探讨了AS发生发展的炎性机制,并从促进、抑制和双向调控AS进展三个方面阐述了其相关的炎性     

白细胞介素37与动脉粥样硬化关系的研究进展

动脉粥样硬化(As)作为一种血管的慢性炎症性疾病,是冠心病、脑梗死、外周血管疾病的主要原因,严重威胁着人类的健康和生命。白细胞介素37是白细胞介素1家族的新型抗炎分子,在炎症性疾病、肿瘤、自身免疫性疾病中发挥抗炎及免疫抑制作用,该作用的发挥可能与白细胞介素18结合蛋白、Smad3相关。目前临床及动物试验均证实白细胞介素37参与了As的病理生理过程,可通过抑制巨噬细胞、肥大细胞、树突状细胞的功能,促进Treg细胞的分化而起到抗As的作用。本文拟对白细胞介素37与As关系的研究进展作一综述。     

IL-18在动脉粥样硬化相关疾病中的研究进展

动脉粥样硬化（atherosclerosis,AS）是心血管系统的慢性炎症性疾病,是缺血性心脏病、脑卒中和周围血管疾病的主要病因之一。越来越多的证据表明,炎症反应是斑块不稳定性及斑块破裂的重要因素,贯穿不稳定斑块的发生、发展及破裂的全过程。白细胞介素18(interleukin-18,IL-18)是一种新型的促炎细胞因子,可以促进炎症反应,是参与动脉粥样硬化炎症进程的重要因子。本文就IL-18在AS发病机制中的作用及其在AS相关疾病中的研究现状作一综述,以期为AS及其相关疾病提供新的检测指标和治疗靶点。     

动脉粥样硬化与炎症

冠状动脉疾病(CAD)是冠状动脉壁内富含胆固醇斑块积聚的结果,是最终导致死亡的主要原因。其中炎症是导致动脉粥样硬化的重要因素之一。因此需要新的靶向抗动脉粥样硬化治疗。本文对炎症在动脉粥样硬化中的作用以及目前正在研究的靶向动脉粥样硬化的抗炎疗法进行综述。     

急性脑梗死病人阿司匹林抵抗与血小板miR-223的相关性研究

目的检测急性脑梗死病人外周血中miR-223的表达水平,探讨其与阿司匹林抵抗的相关性。方法将58例急性脑梗死病人作为病例组,另选取同期60名健康体检者作为对照组,采用实时荧光定量聚合酶链反应(RT-PCR)技术检测两组miR-223的表达水平;利用全血电阻法将病例组分为阿司匹林抵抗组和阿司匹林敏感组,分析两组外周血中miR-223的表达差异。结果急性脑梗死病人外周血中miR-223的表达水平较对照组升高,差异有统计学意义(P<0.001);阿司匹林抵抗组较阿司匹林敏感组外周血中miR-223升高,差异有统计学意义(P<0.001)。结论miR-223的高表达可能与急性脑梗死的发生以及阿司匹林抵抗有关。     

血管外膜炎症和动脉粥样硬化

动脉粥样硬化是一种炎症性疾病的假说已逐渐为人们所接受，然而在对其研究过程中，人们长期把注意力集中于血管内膜。最近证据表明，血管外膜炎症和血管外膜细胞也参与动脉粥样硬化的形成过程。本文拟对血管外膜炎症和动脉粥样硬化的关系作一综述。     

老年动脉粥样硬化患者血清白细胞介素-6水平及氨氯地平对其的影响

动脉粥样硬化(AS)患者血清白细胞介素-6 (IL-6)含量升高,而长效钙离子拮抗剂对AS患者血清IL-6水平的影响各家报道不一.本文通过测定AS患者服用氨氯地平后血清IL-6水平的变化,探讨IL-6在AS发病中的意义及长效钙离子拮抗剂对其的影响.     

miR-206对血管内皮细胞增殖的影响及其机制

目的研究miR-206对血管内皮细胞增殖的影响及其机制,为临床动脉硬化疾病提供新的诊疗方向。方法收集临床病理首次确诊为糖尿病下肢动脉粥样硬化病变的患者病变处动脉内皮组织和正常内皮组织,qPCR检测miR-206的表达;而后通过基础实验研究将HUVEC分为未转染组、miR-206-mimics组和miR-206-inhibitor组,观察转染效率;三组细胞均采用CCK8检测细胞增殖情况,Transwell进行迁移能力评估,流式细胞仪检测细胞周期情况,Western blot检测Cx43表达情况。结果糖尿病动脉硬化患者下肢动脉(均为胫腓动脉)病变处内皮细胞miR-206的mRNA表达较正常组织内皮细胞明显增加(P0.05);HUVEC转染miR-206-mimics后,miR-206表达显著升高(P0.05),转染miR-206-inhibitor后,miR-206表达明显降低(P0.05);在HUVEC转染miR-206-mimics 24 h后,细胞增殖率相比于未转染组和miR-206-inhibitor组要明显降低(P0.05);在HUVEC转染miR-206-mimics后,细胞迁移能力明显降低(P0.05),细胞周期在G2期发生阻滞,而HUVEC转染miR-206-inhibitor后细胞迁移能力提高(P0.05);miR-206-mimics组细胞Cx43表达明显降低,而miR-206-inhibitor组细胞Cx43表达明显增加。结论 miR-206可以抑制血管内皮细胞的增殖,将内皮细胞阻滞在有丝分裂G2期,并且抑制内皮细胞迁移,其对内皮细胞增殖的影响可能是通过调节Cx43表达来实现的。     

miR‐223: infection,inflammation and cancer

Expression of the microRNA miR‐223 is deregulated during influenza or hepatitis B infection and in inflammatory bowel disease, type 2 diabetes, leukaemia and lymphoma. Although this may also be the result of the disease per se, increasing evidence suggests a role for miR‐223 in limiting inflammation to prevent collateral damage during infection and in preventing oncogenic myeloid transformation. Validated targets for miR‐223 that have effects on inflammation and infection include granzyme B, IKKα, Roquin and STAT3. With regard to cancer, validated targets include C/EBPβ, E2F1, FOXO1 and NFI‐A. The effect of miR‐223 on these targets has been documented individually; however, it is more likely that miR‐223 affects multiple targets simultaneously for key processes where the microRNA is important. Such processes include haematopoietic cell differentiation, particularly towards the granulocyte lineage (where miR‐223 is abundant) and as cells progress down the myeloid lineage (where miR‐223 expression decreases). NF‐κB and the NLRP3 inflammasome are important inflammatory mechanisms that are dampened by miR‐223 in these cell types. The miRNA can also directly target viruses such as HIV, leading to synergistic effects during infection. Here we review the recent studies of miR‐223 function to show how it modulates inflammation, infection and cancer development.     

SIRT6 protects against endothelial dysfunction and atherosclerosis in mice

SIRT6 is an important member of sirtuin family that represses inflammation, aging and DNA damage, three of which are causing factors for endothelial dysfunction. SIRT6 expression is decreased in atherosclerotic lesions from ApoE^−/− mice and human patients. However, the role of SIRT6 in regulating vascular endothelial function and atherosclerosis is not well understood. Here we show that SIRT6 protects against endothelial dysfunction and atherosclerosis. Global and endothelium-specific SIRT6 knockout mice exhibited impaired endothelium-dependent vasorelaxation. Moreover, SIRT6^+/− haploinsufficient mice fed a high-fat diet (HFD) also displayed impaired endothelium-dependent vasorelaxation. Importantly, SIRT6^+/−;ApoE^−/− mice after HFD feeding exhibited exacerbated atherosclerotic lesion development, concurrent with increased expression of the proinflammatory cytokine VCAM-1. Loss- and gain-of-SIRT6 function studies in cultured human endothelial cells (ECs) showed that SIRT6 attenuated monocyte adhesion to ECs. RNA-sequencing profiling revealed that SIRT6 overexpression decreased the expression of multiple atherosclerosis-related genes, including proatherogenic gene TNFSF4 (tumor necrosis factor superfamily member 4). Chromatin immunoprecipitation assays showed that SIRT6 decreased TNFSF4 gene expression by binding to and deacetylating H3K9 at TNFSF4 gene promoter. Collectively, these findings demonstrate that SIRT6 play a pivotal role in maintaining endothelial function and increased SIRT6 activity could be a new therapeutic strategy to combat atherosclerotic disease.     

血管周围脂肪组织在动脉粥样硬化炎症发展中的作用

动脉粥样硬化被认为是一个多细胞、多因子参与的慢性炎症性疾病,血管外层在其中发挥了重要作用。血管周围脂肪组织在肥胖、炎症等病理状态下,会通过脂肪细胞表型转化进而释放脂肪因子及炎症因子并调节各类炎症细胞,“从外向内”调控血管的免疫反应,进一步调控动脉粥样硬化。对血管周围脂肪组织进行干预可能是防治动脉粥样硬化的新策略。     

血浆miR-223和Fox03a水平与冠心病及其传统危险因素之间的相关性研究

目的 探讨血浆miR-223和FoxO3a水平与冠心病及传统危险因素之间的相关性.方法 纳入2019年1月至2019年12月在新疆医科大学第一附属医院住院的冠心病患者126例(冠心病组)和非冠心病患者111例(对照组),两组平均年龄为(66.38±12.12)岁和(49.35±9.60)岁.通过酶联免疫分析法,检测所有...     

Modified LDL - trigger of atherosclerosis and inflammation in the arterial intima

Atherosclerosis is characterized by chronic inflammation of an injured intima. The pathological processes are initiated by accumulation of morphologically distinct, modified forms of LDL, and followed by cellular infiltration and foam cell formation. Activated intimal cells secrete enzymes and agents capable of modifying LDL, and the modified lipids of LDL, in turn, are able to activate intimal cells and to trigger various inflammatory signals. These processes can initiate and maintain a vicious circle in the intima and lead to lesion progression. In this review, we focus on the LDL modifications relevant to the initial lipid accumulation and discuss their pro-inflammatory effects.     

Apoptosis in the vascular wall and atherosclerosis

Apoptosis, programmed cell death, has emerged as a key element in the complex pathophysiology underlying the development as well as the progression of atherosclerosis. A number of recent reports provided evidence for both in vivo and in vitro occurrence of apoptotic cell death of vascular cells, namely endothelial cells, macrophages, and vascular smooth muscle cells. In addition, functional studies in disease models underscore the relevance of these findings for the understanding of processes which lead to lesion development, plaque rupture, and thrombus formation. Pathomechanistic in vitro investigations provided an increasingly detailed picture of the involved intracellular signaling pathways that regulate onset and execution of apoptosis. These insights offer the potential of therapeutic interventions targeted to interfere with the molecular processes involving apoptotic cell death in the vascular wall. Received: 18 August 2000, Returned for revision: 30 August 2000, Revision received: 11 September 2000, Accepted: 13 September 2000     

MiR-223-3p affects myocardial inflammation and apoptosis following myocardial infarction via targeting FBXW7

BackgroundMyocardial infarction (MI) is one of the main causes of disability and death in the world, leading to myocarditis and cardiomyocyte apoptosis. Studies have shown that microRNA (miRNA) is involved in myocarditis and apoptosis. The main purpose of this study was to explore the regulatory mechanism of miR-223-3p on myocarditis and apoptosis after MI.MethodsWe cultured H9c2 cells and detected the expression of miR-223-3p in cells treated with different concentrations of H₂O₂. Sprague Dawley (SD) rats were fed with normal diet, constructed an MI model and detect the expression of miR-223-3p in heart tissue. Overexpression or inhibition of miR-223-3p was conducted in MI model cells in vitro, and the contents of the inflammatory factors tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-10 (IL-10) in cell supernatant were detected by enzyme-linked immunosorbent assay (ELISA). Cell apoptosis was detected by flow cytometry. Luciferase activity assay was used to detect the targeting relationship between miR-223-3p and FBXW7, and the expression of FBXW7 in cells was also detected. Overexpression of miR-223-3p was performed in MI rats to detect the expression of inflammatory factors, FBXW7, and apoptosis in rat cardiac tissue.ResultsThe expression of miR-223-3p was down regulated in MI models established in vitro and in vivo. Overexpression of miR-223-3p can inhibit inflammatory response and apoptosis in H9c2 cells and cardiac tissues. It was revealed that miR-223-3p can inhibit the expression of FBXW7, reduce myocarditis and apoptosis after MI, and improve cardiac function.ConclusionsIt is possible that miR-223-3p reduces myocarditis and apoptosis after MI and improves cardiac function by targeted inhibition of FBXW7 expression.