MAFB

MAFB
  • 文章类型: Journal Article
    面部裂痕(OFC)是全球第二大常见的出生缺陷。OFC的病因涉及遗传与环境之间的复杂相互作用。基因组技术的进步已经鉴定了与OFC相关的基因变体。本研究旨在调查MYH9、MTHFR、MAFB,SUMO1基因影响波兰人群中非综合征性OFC的发生。该研究包括209名患有非综合征性OFC的个体和418名健康对照。收集唾液和脐带血样品用于DNA提取。MYH9中的四个SNP,MTHFR,MAFB,和SUMO1基因使用基于实时PCR的TaqMan测定进行基因分型。使用逻辑回归进行统计分析以评估SNP和OFC之间的关联。发现rs7078CC多态性与OFCs之间存在显着相关性(OR=3.22,CI1.68-6.17,p<0.001)。没有发现rs1081131、rs13041247和rs3769817多态性的显著关联。研究表明,rs7078多态性显著影响波兰人群口面腭裂的发生,而rs3769817、rs1801131和rs13041247SNP没有显示出这种相关性。
    Orofacial clefts (OFCs) are the second most common birth defect worldwide. The etiology of OFCs involves complex interactions between genetics and environment. Advances in genomic technologies have identified gene variants associated with OFCs. This study aimed to investigate whether selected SNPs in the MYH9, MTHFR, MAFB, and SUMO1 genes influence the occurrence of non-syndromic OFCs in the Polish population. The study included 209 individuals with non-syndromic OFCs and 418 healthy controls. Saliva and umbilical cord blood samples were collected for DNA extraction. Four SNPs in the MYH9, MTHFR, MAFB, and SUMO1 genes were genotyped using real-time PCR-based TaqMan assays. Statistical analysis was performed using logistic regression to assess the association between SNPs and OFCs. A significant association was found between the rs7078 CC polymorphism and OFCs (OR = 3.22, CI 1.68-6.17, p < 0.001). No significant associations were identified for the rs1081131, rs13041247, and rs3769817 polymorphisms. The research indicates that the rs7078 polymorphism significantly influences the occurrence of orofacial cleft palate in the Polish population, whereas the rs3769817, rs1801131, and rs13041247 SNPs do not show such a correlation.
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  • 文章类型: Journal Article
    目的:本研究的目的是探讨MAFbZIP转录因子B(MAFB)是否可以减轻葡聚糖硫酸钠(DSS)诱导的小鼠和LPS诱导的IEC-6细胞的溃疡性结肠炎(UC)。
    方法:利用DSS和LPS建立UC体内外模型,分别。每天记录小鼠体重和疾病活动指数(DAI)评分,测量结肠长度。此外,利用异硫氰酸荧光素葡聚糖(FITC-葡聚糖)探针评价渗透性。利用H&E染色评估DSS诱导的结肠炎小鼠的组织病理学变化。接下来,qRT-PCR检测IL-1β,IL-6,TNF-α,体内和体外IL-10水平。此外,MDA的水平,SOD,CAT,在结肠组织中评估GSH。此外,免疫印迹法检测结肠炎小鼠和IEC-6细胞中紧密连接蛋白和NF-κB通路相关蛋白的表达,免疫组织化学和免疫荧光。
    结果:在DSS诱导的结肠炎小鼠中,MAFB水平下调。此外,MAFB的上调通过抑制DSS诱导的炎症保护小鼠免受DSS诱导的结肠炎,氧化应激,肠屏障受损。我们还证明了在DSS引起的结肠炎小鼠中,MAFB的上调使NF-κB途径失活。随后,我们观察到MAFB上调可抑制LPS引起的IEC-6细胞上皮屏障损伤和炎症反应。此外,MAFB过表达可抑制IEC-6细胞NF-κB通路的激活。
    结论:MAFB的上调可能通过抑制NF-κB通路抑制炎症和肠屏障损伤来保护UC。
    OBJECTIVE: The aim of this study was to explore whether MAF bZIP transcription factor B (MAFB) might alleviate ulcerative colitis (UC) in dextran sulfate sodium (DSS)-induced mice and LPS-induced IEC-6 cells.
    METHODS: UC in vivo and in vitro model was established by using DSS and LPS, respectively. The mice body weight and disease activity index (DAI) score were recorded daily, and colon length was measured. Moreover, the permeability was evaluated utilizing a fluorescein isothiocyanate dextran (FITC-Dextran) probe. Histopathological changes of DSS-induced colitis mice was assessed utilizing H&E staining. Next, qRT-PCR was performed to detect IL-1β, IL-6, TNF-α, and IL-10 level in in vivo and in vitro. Furthermore, the level of MDA, SOD, CAT, and GSH were evaluated in colon tissues. Besides, the expressions of tight junction proteins and NF-κB pathway relative proteins were examined in colitis mice and IEC-6 cells using western blot, immunohistochemistry and immunofluorescence.
    RESULTS: MAFB level was downregulated in DSS-induced colitis mice. Moreover, the upregulation of MAFB protected mice from DSS-induced colitis by suppressing DSS-induced inflammation, oxidative stress, and intestinal barrier impairment. We also demonstrated that the upregulation of MAFB inactivated NF-κB pathway in DSS-caused colitis mice. Subsequently, we observed that MAFB upregulation could inhibit LPS-caused epithelial barrier impairment and inflammation in IEC-6 cells. Additionally, MAFB overexpression could suppress the activation of NF-κB pathway in IEC-6 cells.
    CONCLUSIONS: The upregulation of MAFB could protect against UC via the suppression of inflammation and the intestinal barrier impairment through inhibiting the NF-κB pathway.
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  • 文章类型: Journal Article
    MafB是调节巨噬细胞分化的转录因子。巨噬细胞是仓鼠Harderian腺(HG)的传统特征;但是,关于MafB在HG中表达的研究很少。这里,对仓鼠中MafB基因的全长cDNA进行克隆和测序。分子特征显示MafB编码含有323个氨基酸的蛋白质,具有DNA结合域,一个反式激活域,和一个亮氨酸拉链域。qPCR测定表明MafB在两种性别的不同组织中表达。在胰腺中鉴定出内分泌组织中的最高相对表达水平。雄性仓鼠的性腺切除术与HG中mRNA水平显着升高有关;用二氢睾酮替代可恢复mRNA表达。雄性仓鼠的HG比雌性仓鼠的HG包含两倍多的MafBmRNA。肾上腺在发情周期中显示出相似的mRNA相对表达水平。发情期与卵巢中较高的mRNA水平有关。在胰腺中发现了MafB的显着上调表达和性二态。因此,HG中的MafB可能在吞噬活性和眼内修复所需的巨噬细胞分化中起积极作用。此外,性类固醇似乎强烈影响HG和胰腺中MafB的表达。这些研究强调了MafB在免疫防御和胰腺β细胞调节中可能的生物学重要性。
    MafB is a transcription factor that regulates macrophage differentiation. Macrophages are a traditional feature of the hamster Harderian gland (HG); however, studies pertaining to MafB expression in the HG are scant. Here, the full-length cDNA of the MafB gene in hamsters was cloned and sequenced. Molecular characterization revealed that MafB encodes a protein containing 323 amino acids with a DNA-binding domain, a transactivation domain, and a leucine zipper domain. qPCR assays indicated that MafB was expressed in different tissues of both sexes. The highest relative expression levels in endocrine tissues were identified in the pancreas. Gonadectomy in male hamsters was associated with significantly higher mRNA levels in the HG; replacement with dihydrotestosterone restored mRNA expression. The HG in male hamsters contained twofold more MafB mRNA than the HG of female hamsters. Adrenals revealed similar mRNA relative expression levels during the estrous cycle. The estrous phase was associated with higher mRNA levels in the ovary. A significantly up-regulated expression and sexual dimorphism of MafB was found in the pancreas. Therefore, MafB in the HG may play an active role in the macrophage differentiation required for phagocytosis activity and intraocular repair. Additionally, sex steroids appear to strongly influence the MafB expression in the HG and pancreas. These studies highlight the probable biological importance of MafB in immunological defense and pancreatic β cell regulation.
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  • 文章类型: Journal Article
    变应性鼻炎(AR)是一种常见的过敏性疾病。细胞色素P450,家族2,亚家族e,多肽1(Cyp2e1)是细胞色素P450酶家族的成员,虽然它在AR中的作用仍在揭晓。在AR小鼠中,Cyp2e1的T细胞特异性过表达缓解了AR症状。过表达Cyp2e1抑制小鼠鼻黏膜嗜酸性粒细胞和肥大细胞的浸润,和鼻腔灌洗液(NALF)中的炎症细胞。Cyp2e1过表达小鼠的杯状细胞增生和粘液分泌减少,鼻粘膜中MUC5AC表达减少。Cyp2e1过表达后,AR小鼠鼻黏膜上皮通透性和完整性得到改善,血清中异硫氰酸荧光素-葡聚糖4含量降低,NALF中IL-25,IL-33和TSLP的表达增加,鼻粘膜中ZO-1的表达和阻塞增加。Cyp2e1通过降低NALF或鼻粘膜中IL-4,IL-5和IL-13的表达和分泌以及GATA-3的表达来抑制Th2免疫应答。我们证明Cyp2e1抑制了初始CD4+T细胞向Th2亚型的分化,通过与Cyp2e1启动子结合激活其转录而受MAFB调控。总的来说,这些结果表明Cyp2e1通过抑制CD4+T细胞向Th2细胞分化来缓解AR症状的潜在作用。我们的发现为AR机制提供了进一步的见解。
    Allergic rhinitis (AR) is a common allergic disease. Cytochrome P450, family 2, subfamily e, polypeptide 1 (Cyp2e1) is a member of the cytochrome P450 family of enzymes, while its role in AR is still unveiled. In AR mice, T cell-specific overexpression of Cyp2e1 relieved the AR symptoms. Overexpressed-Cyp2e1 restrained the infiltration of eosinophils and mast cells in the nasal mucosa of mice, and the inflammatory cells in nasal lavage fluid (NALF). Cyp2e1 overexpressed mice exhibited decreased goblet cell hyperplasia and mucus secretion as well as decreased MUC5AC expression in nasal mucosa. The epithelial permeability and integrity of nasal mucosa were improved upon Cyp2e1 overexpression in AR mice, as evidenced by decreased fluorescein isothiocyanate-dextran 4 content in serum, increased expression of IL-25, IL-33, and TSLP in NALF, and increased expression of ZO-1 and occluding in nasal mucosa. Cyp2e1 inhibited Th2 immune response by decreasing the expression and secretion of IL-4, IL-5, and IL-13 as well as the expression of GATA-3 in NALF or nasal mucosa. We proved that Cyp2e1 inhibited the differentiation of naïve CD4+ T cells toward the Th2 subtype, which was regulated by MAFB by binding to Cyp2e1 promoter to activate its transcription. Overall, these results show the potential role of Cyp2e1 in alleviating AR symptoms by restraining CD4+ T cells to Th2 cell differentiation. Our findings provide further insight into the AR mechanism.
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  • 文章类型: Journal Article
    免疫细胞介导的慢性炎症是2型糖尿病(T2DM)的病因之一。因此,确定循环免疫细胞中的炎症标志物对于预测胰岛素抵抗(IR)和T2DM的发生具有重要意义。在这项研究中,我们通过批量转录组测序(bulkRNA-seq)发现,T2DM患者外周血单个核细胞(PBMC)中的差异表达基因(DEGs)与先天免疫和慢性炎症反应相关.基因整合分析显示9个DEGs上调,和受试者工作特征(ROC)曲线分析显示,V-maf肌膜膜纤维肉瘤癌基因同源物B(MAFB),候选生物标志物,对T2DM有一定的预测价值。在基于人群的队列研究中,我们发现,在T2DM患者的PBMC中,MAFB表达显著上调,并且与IR的稳态模型评估(HOMA-IR)显著相关,肿瘤坏死因子-α(TNF-α),脂联素(Adipoq),等。我们进一步评估了MAFB和其他临床参数预测和诊断T2DM的敏感性和特异性,发现PBMC中MAFB的表达对T2DM的预测和诊断具有积极作用。最后,单细胞RNA测序(scRNA-seq)分析显示,MAFB表达的增加主要是在非经典单核细胞中。我们的结果表明,循环单核细胞中MAFB表达的增加可能介导T2DM患者的慢性炎症状态。因此,循环单核细胞MAFB基因的表达对预测和辅助诊断T2DM具有一定的临床意义。
    Immune cell-mediated chronic inflammation is one of the causes of type 2 diabetes mellitus (T2DM). Therefore, identifying inflammatory markers in circulating immune cells is highly important for predicting insulin resistance (IR) and the occurrence of T2DM. In this study, we discovered that differentially expressed genes (DEGs) in peripheral blood mononuclear cells (PBMCs) from T2DM patients were associated with innate immunity and chronic inflammatory responses through bulk transcriptome sequencing (bulk RNA-seq). Gene integration analysis revealed that nine DEGs were upregulated, and receiver operating characteristic (ROC) curve analysis revealed that V-maf musculoaponeurotic fibrosarcoma oncogene homolog B (MAFB), a candidate biomarker, has a certain predictive value for T2DM. In population-based cohort studies, we found that MAFB expression was significantly upregulated in the PBMCs of T2DM patients and was significantly correlated with homeostasis model assessment of IR (HOMA-IR), tumor necrosis factor-α (TNF-α), adiponectin (Adipoq), etc. We further evaluated the sensitivity and specificity of MAFB and other clinical parameters for predicting and diagnosing T2DM and found that MAFB expression in PBMCs had a positive effect on the prediction and diagnosis of T2DM. Finally, single-cell RNA sequencing (scRNA-seq) analysis revealed that the increase in MAFB expression was mainly in nonclassical monocytes. Our results suggest that increased MAFB expression in circulating monocytes may mediate chronic inflammatory status in patients with T2DM. Therefore, MAFB gene expression in circulating monocytes has certain clinical significance for predicting and assisting in the diagnosis of T2DM.
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  • 文章类型: Case Reports
    多中心腕骨骨溶解综合征(MCTO)是一种罕见的骨骼疾病,其特征是累及腕骨和tal骨的进行性骨溶解,常与肾病有关。它是由MAFbZIP转录因子B(MAFB)基因的杂合突变引起的。在MCTO患者中已经观察到不同的临床表现和广泛的疾病严重程度。这里,我们报告了一例男性患者,该患者在儿童期出现肾衰竭,并伴有进行性致残性骨骼畸形。他31岁时被诊断出患有MCTO,其中鉴定了MAFB基因的NM_005461.5:c.212C>A:p。(Pro71His)中的从头致病性杂合变体。虽然关于这种疾病的长期预后和预期寿命的数据很少,本病例报告揭示了一名MCTO患者在33年的一生中出现多种重大疾病的衰弱病程.
    Multicentric carpotarsal osteolysis syndrome (MCTO) is a rare skeletal disorder characterized by progressive osteolysis involving the carpal and tarsal bones, and often associated with nephropathy. It is caused by heterozygous mutation in the MAF bZIP transcription factor B (MAFB) gene. Heterogeneous clinical manifestation and wide spectrum of disease severity have been observed in patients with MCTO. Here, we report a case of a male patient who presented with kidney failure in childhood with progressive disabling skeletal deformity. He was diagnosed with MCTO at 31-years-old, where a de novo pathogenic heterozygous variant in NM_005461.5:c.212C>A: p.(Pro71His) of the MAFB gene was identified. While there has been little data on the long-term prognosis and life expectancy of this disease, this case report sheds light on the debilitating disease course with multiple significant morbidities of a patient with MCTO throughout his lifetime of 33 years.
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  • 文章类型: Journal Article
    单核细胞来源的巨噬细胞在炎症性疾病中起着关键的致病作用。在类风湿性关节炎(RA)的情况下,特定滑膜组织浸润巨噬细胞亚群的存在与活动性疾病或炎症消退有关.JAK抑制剂(JAKi)是第一个被批准用于治疗RA的靶向合成疾病缓解抗风湿药(tsDMARD),其疗效与生物制剂相当。然而,JAKi对巨噬细胞特化和分化的影响目前尚不清楚.我们分析了JAKi对RA患者外周血单核细胞亚群的转录和功能影响,以及对粒细胞-巨噬细胞集落刺激因子(GM-CSF)促进的单核细胞衍生巨噬细胞分化的影响,是推动RA发展和发病的因素。我们现在报道,JAKiUpadacitinib恢复了RA患者外周血单核细胞亚群的平衡,并以剂量依赖的方式使巨噬细胞偏向于获得抗炎转录和功能谱。Upadacitinib处理的巨噬细胞显示出定义与稳态/炎症消退相关的滑膜巨噬细胞的基因的强阳性富集。具体来说,Upadacitinib处理的巨噬细胞显示MAFB和MAFB调节基因的表达显着升高,GSK3β的抑制磷酸化升高,和更高的吞噬活性,并在病原刺激激活后显示出抗炎细胞因子谱。这些结果也由暴露于其他JAKI(baricitinib,托法替尼),但不存在TYK2抑制剂deucravitinib。作为一个整体,我们的结果表明,JAKi促进巨噬细胞重编程,以获得更多的抗炎/促分辨率谱,与JAKi增强MAFB表达能力相关的作用。
    Monocyte-derived macrophages play a key pathogenic role in inflammatory diseases. In the case of rheumatoid arthritis (RA), the presence of specific synovial tissue-infiltrating macrophage subsets is associated with either active disease or inflammation resolution. JAK inhibitors (JAKi) are the first targeted synthetic disease-modifying antirheumatic drugs (tsDMARD) approved for treatment of RA with comparable efficacy to biologics. However, the effects of JAKi on macrophage specification and differentiation are currently unknown. We have analyzed the transcriptional and functional effects of JAKi on human peripheral blood monocyte subsets from RA patients and on the differentiation of monocyte-derived macrophages promoted by granulocyte-macrophage colony-stimulating factor (GM-CSF), a factor that drives the development and pathogenesis of RA. We now report that JAKi Upadacitinib restores the balance of peripheral blood monocyte subsets in RA patients and skewed macrophages towards the acquisition of an anti-inflammatory transcriptional and functional profile in a dose-dependent manner. Upadacitinib-treated macrophages showed a strong positive enrichment of the genes that define synovial macrophages associated to homeostasis/inflammation resolution. Specifically, Upadacitinib-treated macrophages exhibited significantly elevated expression of MAFB and MAFB-regulated genes, elevated inhibitory phosphorylation of GSK3β, and higher phagocytic activity and showed an anti-inflammatory cytokine profile upon activation by pathogenic stimuli. These outcomes were also shared by macrophages exposed to other JAKi (baricitinib, tofacitinib), but not in the presence of the TYK2 inhibitor deucravacitinib. As a whole, our results indicate that JAKi promote macrophage re-programming towards the acquisition of a more anti-inflammatory/pro-resolution profile, an effect that correlates with the ability of JAKi to enhance MAFB expression.
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  • 文章类型: Journal Article
    转录因子MAFB调节巨噬细胞的各种稳态功能。这项研究探讨了MAFB在使用巨噬细胞特异性Mafb缺陷(Mafbf/f::LysM-Cre)小鼠的棕色脂肪组织(BAT)产热中的作用。我们发现巨噬细胞中的Mafb缺乏会减少产热,能量消耗,在寒冷条件下,BAT中的交感神经元(SN)密度。这种表型的特点是以巨噬细胞/粒细胞积累为特征的促炎环境,白细胞介素-6(IL-6)的产生增加,和IL-6反式信号,导致BAT中神经生长因子(NGF)表达减少和SN密度降低。我们在RAW-264.7巨噬细胞系中使用由IL-6启动子驱动的荧光素酶读出来确认IL-6表达的MAFB调节。免疫组织化学显示BAT中NGF产生细胞的聚集组织,主要是TRPV1+血管平滑肌细胞,如使用单细胞RNA测序和基质血管部分的RT-qPCR所显示的。用抗IL-6受体抗体治疗Mafbf/f::LysM-Cre小鼠可以挽救SN密度,体温,和能量消耗。
    Transcription factor MAFB regulates various homeostatic functions of macrophages. This study explores the role of MAFB in brown adipose tissue (BAT) thermogenesis using macrophage-specific Mafb-deficient (Mafbf/f::LysM-Cre) mice. We find that Mafb deficiency in macrophages reduces thermogenesis, energy expenditure, and sympathetic neuron (SN) density in BAT under cold conditions. This phenotype features a proinflammatory environment that is characterized by macrophage/granulocyte accumulation, increases in interleukin-6 (IL-6) production, and IL-6 trans-signaling, which lead to decreases in nerve growth factor (NGF) expression and reduction in SN density in BAT. We confirm MAFB regulation of IL-6 expression using luciferase readout driven by IL-6 promoter in RAW-264.7 macrophage cell lines. Immunohistochemistry shows clustered organization of NGF-producing cells in BAT, which are primarily TRPV1+ vascular smooth muscle cells, as additionally shown using single-cell RNA sequencing and RT-qPCR of the stromal vascular fraction. Treating Mafbf/f::LysM-Cre mice with anti-IL-6 receptor antibody rescues SN density, body temperature, and energy expenditure.
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  • 文章类型: Journal Article
    半乳糖凝集素-9(Gal-9)在类风湿关节炎(RA)发病机制中的作用尚不清楚。本研究旨在探讨Gal-9在RA中的作用机制和治疗潜力。我们在临床样本中检测到Gal-9表达,探讨Gal-9在成纤维细胞样滑膜细胞(FLSs)中的敲低和过表达,并在胶原诱导性关节炎(CIA)模型中进一步验证。我们发现,RA滑膜中的Gal-9水平明显高于骨关节炎患者(OA)。在RA患者的血浆中肿瘤坏死因子(TNF-α)抑制剂治疗后,Gal-9显着降低。此外,转录组测序显示Gal-9参与TNF-α途径的调节。在FLSs中,TNF-α刺激后Gal-9显著上调,Gal-9基因敲低可显著抑制TNF-α激活的增殖,迁移和炎症反应。根据细胞转录组测序结果,我们进一步证实Gal-9可以通过与MAFB相互作用并影响PI3K/AKT/mTOR通路来实现这些作用.最后,我们在CIA模型上降低了Gal-9,发现它可以缓解关节炎的进展。总之,我们的研究表明,敲低Gal-9可以通过MAFB抑制TNF-α诱导的RA激活,PI3K/AKT/mTOR。
    The role of Galectin-9 (Gal-9) in the pathogenesis of rheumatoid arthritis (RA) remains unclear. This study aimed to investigate the mechanism of action and therapeutic potential of Gal-9 in RA. We detected Gal-9 expression in clinical samples, explored the mechanism of function of Gal-9 by knockdown and overexpression in fibroblast-like synoviocytes (FLSs), and further verified it in collagen-induced arthritis (CIA) model. We found that the levels of Gal-9 were considerably elevated in RA synovium than in osteoarthritis (OA) patients. A substantial decrease of Gal-9 was demonstrated after tumor necrosis factor (TNF-α) inhibitor treatment in the plasma of patients with RA. Additionally, transcriptome sequencing revealed that Gal-9 was involved in the regulation of the TNF-α pathway. Gal-9 was considerably upregulated after TNF-α stimulation in FLSs, and knockdown of Gal-9 substantially inhibited TNF-α activated proliferation, migration and inflammatory response. According to cell transcriptome sequencing results, we further confirmed that Gal-9 could achieve these effects by interacting with MAFB and affecting PI3K/AKT/mTOR pathway. Finally, we knocked down Gal-9 on the CIA model and found that it could alleviate the progression of arthritis. In conclusion, our study revealed that the knockdown of Gal-9 could inhibited TNF-α induced activation in RA through MAFB, PI3K/AKT/mTOR.
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  • 文章类型: Journal Article
    茶和茶产品被广泛用作世界上最受欢迎的饮料。EGCG是绿茶中生物活性最丰富的茶多酚,对糖尿病的预防和治疗有积极作用。然而,EGCG暴露对成年小鼠葡萄糖稳态和胰岛的影响尚未有报道.在这项研究中,我们研究了成年雄性小鼠在饮用水中暴露于1和10mg/kg/天EGCG60天后的葡萄糖稳态以及胰岛α和β细胞的形态和分子变化。两个EGCG组均未影响葡萄糖稳态。胰腺十二指肠同源盒1(Pdx1)在β细胞中的表达上调,这可能与胰岛素水平升高有关,10mg/kg/天EGCG组的β细胞量和β细胞增殖。Aristaless相关同源异型盒(Arx)在α细胞中的表达无明显变化,这与不变的α细胞质量相对应。在两个EGCG组中,肌腱膜纤维肉瘤癌基因同源物B(MafB)阳性α细胞的显着减少可能与胰高血糖素水平降低有关。这些结果表明,EGCG补充剂量依赖性增加成年小鼠的β细胞质量,并影响血清胰岛素和胰高血糖素的水平。我们的结果表明,健康人经常喝茶可能有预防糖尿病的可能性。
    Tea and tea products are widely used as the most popular beverage in the world. EGCG is the most abundant bioactive tea polyphenol in green tea, which has positive effects on the prevention and treatment of diabetes. However, the impact of EGCG exposure on glucose homeostasis and islets in adult mice have not been reported. In this study, we studied glucose homeostasis and the morphological and molecular changes of pancreatic islet α and β cells in adult male mice after 60 d of exposure to 1 and 10 mg/kg/day EGCG by drinking water. Glucose homeostasis was not affected in both EGCG groups. The expression of pancreatic duodenal homebox1 (Pdx1) in β cells was upregulated, which might be related to increased insulin level, β cell mass and β cell proliferation in 10 mg/kg/day EGCG group. The expression of aristaless-related homeobox (Arx) in α cells did not change significantly, which corresponded with the unchanged α-cell mass. The significant reduction of musculoaponeurotic fibrosarcoma oncogene homolog B (MafB) positive α-cells might be associated with decreased glucagon level in both EGCG groups. These results suggest that EGCG supplementation dose-dependent increases β cell mass of adult mice and affects the levels of serum insulin and glucagon. Our results show that regular tea drinking in healthy people may have the possibility of preventing diabetes.
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