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Correlation exploration among CT imaging, pathology and genotype of pulmonary ground-glass opacity 肺毛玻璃样混浊的CT影像、病理与基因型的相关性探讨
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-20 DOI: 10.1111/jcmm.17797
Yong Cai, Tong Chen, Shiju Zhang, Min Tan, Jiying Wang
<p>To analyse the clinical features, imaging manifestation, pathological typing and genetic testing results of patients undergoing surgery for ground-glass opacity (GGO) nodules, and explore the reasonable diagnosis and treatment program for GGO patients as to provide the basis for the establishment of GGO treatment process. This study is an exploratory study. 465 cases with GGO confirmed by HRCT, undergoing surgery and approved by pathologic diagnosis in Shanghai pulmonary hospital were enrolled in this study. All the patients with GGO were cases with single lesion. The relationship between the clinical, imaging, pathological and molecular biological data of single GGO were statistically studied. (1) Among 465 cases, the median age was 58 years and females were 315 (67.7%); there were 397 (85.4%) non-smoking, and 354 cases (76.1%) had no clinical symptoms. There were 33 cases of benign and 432 cases of malignant GGO. Significant differences were observed on the size, vacuole sign, pleural indentation and blood vessel sign of GGO between two groups (<i>p</i> < 0.05). Of 230 mGGO, there were no AAH, 13 cases of AIS, 25 cases of MIA and 173 cases of invasive adenocarcinoma. The probability of solid nodules in invasive adenocarcinoma was higher than that in micro invasive carcinoma, and the difference was statistically significant (<i>p</i> < 0.05). 360 cases were followed up with the average follow-up time of 6.05 months, and GGO of 34 cases (9.4%) increased. (2) In 428 adenocarcinoma samples approved by pathologic diagnosis, there were 262 (61.2%) lesions of EGFR mutation, 14 (3.3%) lesions of KRAS mutation, 1 (0.2%) lesion of Braf mutation, 9 (2.1%) lesions of EML4-ALK gene fusion and 2 (0.5%) lesions of ROS1 fusion. The detection rate of gene mutation in mGGO was higher than that of pGGO. During the follow-up period, genetic testing results of 32 GGO showed that EGFR mutation rate was 53.1%, ALK positive rate of 6.3%, KRAS mutation rate of 3.1% and no ros1 and BRAF gene mutation. No statistically significant difference was observed in comparison with unchanged GGO. (3) EGFR mutation rate of invasive adenocarcinoma was the highest (168/228, 73.7%), mainly in the 19Del and L858R point mutations. No KRAS mutation was found in atypical adenoma hyperplasia. No significant difference was observed on the mutation rate of KRAS between different types of GGO (<i>p</i> = 0.811). EML4-ALK fusion gene was mainly detected in invasive adenocarcinoma (7/9). GGO tends to occur in young, non-smoking women. The size of GGO is related to the degree of malignancy. Pleural depression sign, vacuole sign and vascular cluster sign are all characteristic images of malignant GGO. pGGO and mGGO reflect the pathological development of GGO. During the follow-up, it is found that GGO increases and solid components appear, which is the indication of surgical resection. The detection rate of EGFR mutations in mGGO and invasive adenocarcinoma is high. pGGO has heterogenei
分析磨玻璃样混浊(GGO)结节手术患者的临床特点、影像学表现、病理分型和基因检测结果,探讨GGO患者合理的诊断和治疗方案,为制定GGO治疗方案提供依据。本研究是一项探索性研究。本研究纳入465例经HRCT证实,在上海市肺科医院接受手术并经病理证实的GGO患者。所有GGO患者均为单一病变病例。对单个GGO的临床、影像学、病理学和分子生物学数据之间的关系进行了统计研究。(1) 在465例病例中,中位年龄为58岁 女性315例(67.7%);非吸烟者397例(85.4%),无临床症状354例(76.1%)。良性GGO 33例,恶性GGO 432例。GGO的大小、液泡征、胸膜凹陷和血管征两组比较有显著性差异(p <; 在230mGGO中,没有AAH,有13例AIS,25例MIA和173例浸润性腺癌。浸润性腺癌发生实体结节的概率高于微浸润性癌,差异有统计学意义(p <; 随访360例,平均随访时间6.05 GGO增加34例(9.4%)。(2) 经病理诊断的428例腺癌标本中,EGFR突变262例(61.2%),KRAS突变14例(3.3%),Braf突变1例(0.2%),EML4-ALK基因融合9例(2.1%),ROS1融合2例(0.5%)。mGGO的基因突变检出率高于pGGO。随访期间,32例GGO的基因检测结果显示,EGFR突变率为53.1%,ALK阳性率为6.3%,KRAS突变率为3.1%,无ros1和BRAF基因突变。与未改变的GGO相比,没有观察到统计学上的显著差异。(3) 侵袭性腺癌的EGFR突变率最高(168/228,73.7%),主要发生在19Del和L858R点突变中。非典型腺瘤增生中未发现KRAS突变。不同类型GGO的KRAS突变率无显著差异(p = EML4-ALK融合基因主要在侵袭性腺癌中表达(7/9)。GGO往往发生在不吸烟的年轻女性身上。GGO的大小与恶性程度有关。胸膜凹陷征、液泡征和血管簇征均为恶性GGO的特征性影像。pGGO和mGGO反映了GGO的病理发展。随访中发现GGO增加,出现实体成分,是手术切除的指征。mGGO和浸润性腺癌中EGFR突变的检出率较高。pGGO在影像学、病理学和分子生物学方面具有异质性。异质性研究有助于制定正确的个体化诊断和治疗计划。
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引用次数: 1
Schisandra extract ameliorates arthritis pathogenesis by suppressing the NF-κB and MAPK signalling pathways 五味子提取物通过抑制NF-κB和MAPK信号通路改善关节炎的发病机制
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-20 DOI: 10.1111/jcmm.17814
Seong Jae Han, Hyemi Lee, Jiho Nam, Cheol-Ho Pan, Jimin Jeon, Siyoung Yang

Schisandra chinensis is a medicinal plant used to treat various diseases. Extracts from the leaves or fruits of S. chinensis and their components are used in osteoarthritis (OA). The OA inhibitory effect of schisandrol A, one of its components, has been previously confirmed. We aimed to confirm the OA inhibitory effect of Schisandra (including components like schisandrol A) to identify why the inhibitory effect of the Schisandra extract is better. First, we investigated the effects of the Schisandra extract on OA as a potential therapeutic. Experimental OA was induced in a mouse model via destabilized medial meniscus surgery. The animals were orally administered the Schisandra extract; the inhibition of cartilage destruction was confirmed using histological analysis. In vitro analysis showed that the Schisandra extract attenuated osteoarthritic cartilage destruction by regulating IL-1β-induced MMP3 and COX-2 levels. The Schisandra extract inhibited IL-1β-induced degradation of IκB (NF-κB pathway) and IL-1β-induced phosphorylation of p38 and JNK (mitogen-activated protein kinase (MAPK) pathway). RNA-sequencing analysis showed that the Schisandra extract decreased the expression of IL-1β-induced MAPK and NF-κB signalling pathway-related genes more than schisandrol A alone. Therefore, Schisandra extract may be more effective than schisandrol A in preventing OA progression by regulating MAPK and NF-κB signalling.

五味子是一种用于治疗多种疾病的药用植物。五味子叶或果实提取物及其成分用于治疗骨关节炎(OA)。其成分之一五味子酚A的OA抑制作用已被证实。我们的目的是确认五味子(包括五味子酚A等成分)对OA的抑制作用,以确定为什么五味子提取物的抑制效果更好。首先,我们研究了五味子提取物对OA的潜在治疗作用。通过不稳定内侧半月板手术诱导小鼠实验性骨关节炎模型。动物口服五味子提取物;通过组织学分析证实了对软骨破坏的抑制作用。体外分析表明,五味子提取物通过调节il -1β诱导的MMP3和COX-2水平,减轻骨关节炎软骨破坏。五味子提取物抑制il -1β诱导的i -κB降解(NF-κB通路)和il -1β诱导的p38和JNK(丝裂原活化蛋白激酶(MAPK)通路)磷酸化。rna测序分析显示,五味子提取物比五味子酚A更能降低il -1β诱导的MAPK和NF-κB信号通路相关基因的表达。因此,五味子提取物可能比五味子酚A更有效地通过调节MAPK和NF-κB信号传导来阻止OA的进展。
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引用次数: 0
Scutellarin inhibits the glioma cell proliferation by downregulating BIRC5 to promote cell apoptosis 黄芩苷通过下调BIRC5促进胶质瘤细胞凋亡抑制胶质瘤细胞增殖
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-20 DOI: 10.1111/jcmm.17788
Feng Wang, Ma-ChiCheng Bao, Jing Xu, Lan-Lan Shi, Rui-Ze Niu, Ting-Hua Wang, Jia Liu

The expression changes of baculovirus inhibitor of apoptosis repeat-containing protein5 in brain glioma after administration of Scutellarin was detected. To explore the effort of scutellarin on anti-glioma by downregulating BIRC5.The effect of scutellarin on tumour growth and animal survival was detected by administering scutellarin to nude mice subcutaneous tumour formation and SD rats in situ tumour formation models. A significantly different gene BIRC5 was found by using the combination of TCGA databases and network pharmacology. And then qPCR was performed to detect the expression of BIRC5 in glioma tissues, cells and normal brain tissues and glial cells. CCK-8 was used to detect the IC50 of scutellarin on glioma cells. The wound healing assay, flow cytometry and MTT test were used to detect the effect of scutellarin on the apoptosis and proliferation of glioma cells. The expression of BIRC5 in glioma tissues was significantly higher than that in normal brain tissues. Scutellarin can significantly reduce tumour growth and improve animal's survival. After scutellarin was administered, the expression of BIRC5 in U251 cells was significantly reduced. And after same time, apoptosis increased and cell proliferation was inhibited. This original research showed that scutellarin can promote the apoptosis of glioma cells and inhibit the proliferation by downregulating the expression of BIRC5.

检测了给药后脑胶质瘤中杆状病毒抑制细胞凋亡重复序列蛋白5的表达变化。探讨黄芩素通过下调BIRC5抗胶质瘤的作用。通过裸鼠皮下肿瘤形成模型和SD大鼠原位肿瘤形成模型,观察黄芩苷对肿瘤生长和动物存活的影响。结合TCGA数据库和网络药理学,发现BIRC5基因存在显著差异。然后用qPCR检测BIRC5在胶质瘤组织、细胞和正常脑组织、胶质细胞中的表达。CCK-8检测黄芩苷对胶质瘤细胞的IC50。采用创面愈合实验、流式细胞术和MTT法检测黄芩苷对胶质瘤细胞凋亡和增殖的影响。BIRC5在胶质瘤组织中的表达明显高于正常脑组织。黄芩苷能显著抑制肿瘤生长,提高动物存活率。给药后,U251细胞中BIRC5的表达明显降低。同一时间后,细胞凋亡增加,细胞增殖受到抑制。本研究发现,黄芩苷通过下调BIRC5的表达,促进胶质瘤细胞凋亡,抑制胶质瘤细胞增殖。
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引用次数: 0
Interleukin-13 contributes to the occurrence of oral submucosal fibrosis 白细胞介素-13参与口腔黏膜下纤维化的发生
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-19 DOI: 10.1111/jcmm.17761
Liping Wang, Zhangui Tang, Junhui Huang

Oral submucous fibrosis (OSF) is a chronic progressive fibrosis disease that affects in oral mucosal tissues. Interleukin (IL)-13 has been implicated in the development of fibrosis in multiple organs. Indeed, it contributes to diseases such as pulmonary fibrosis, liver cirrhosis among others. Currently, its expression in OSF and the specific mechanisms are not well understood. The aim of this study was to investigate the role of IL-13 in OSF and further explore whether IL-13 regulates—polarization of M2-macrophages in OSF. Initially, in the tissues of patients with OSF, we observed a high expression of M2-macrophages and IL-13 protein. Additionally, we found a correlation between the expression of IL-13 and the stage of OSF. Arecoline inhibited the proliferation of fibroblasts (FBs) and promoted IL-13 production in vitro. Furthermore, our observations revealed that M2-macrophages increased upon co-culturing M0-macrophages with supernatants containing the IL-13 cytokine. In conclusion, our study demonstrated that arecoline stimulates FBs leading to increased secretion of IL-13, which in turn IL-13 leads to polarization of M2-macrophages and promotes the occurrence of OSF. This suggests that IL-13 may be a potential therapeutic target of OSF.

口腔黏膜下纤维化(OSF)是一种影响口腔粘膜组织的慢性进行性纤维化疾病。白细胞介素(IL)-13与多器官纤维化的发生有关。事实上,它会导致肺纤维化、肝硬化等疾病。目前,其在OSF中的表达及具体机制尚不清楚。本研究旨在探讨IL-13在OSF中的作用,并进一步探讨IL-13是否在OSF中调控m2 -巨噬细胞的极化。最初,在OSF患者的组织中,我们观察到m2 -巨噬细胞和IL-13蛋白的高表达。此外,我们发现IL-13的表达与OSF的分期之间存在相关性。槟榔碱抑制体外成纤维细胞增殖,促进IL-13的产生。此外,我们的观察显示,m0 -巨噬细胞与含有IL-13细胞因子的上清共培养后,m2 -巨噬细胞增加。综上所述,我们的研究表明槟油碱刺激FBs导致IL-13分泌增加,IL-13分泌增加导致m2 -巨噬细胞极化,促进OSF的发生。这表明IL-13可能是OSF的潜在治疗靶点。
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引用次数: 2
Effects of selective cyclooxygenase-2 inhibitor robenacoxib on primary cells derived from feline injection-site sarcoma 选择性环氧合酶-2抑制剂罗苯那昔布对猫注射部位肉瘤原代细胞的影响
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-19 DOI: 10.1111/jcmm.17717
Chen-Hui Lu, Shu-Han Yu, Ching-Ho Wu, Jason Lih-Seng Yeh, Hui-Wen Chang, Chian-Ren Jeng, Yen-Chen Chang

Feline injection-site sarcomas (FISSs) are highly invasive malignant mesenchymal neoplasms that arise from injection sites in cats. Although the tumorigenesis of FISSs is still uncertain, there is a consensus that FISS is associated with chronic inflammation caused by irritation of injection-related trauma and foreign chemical substances. Chronic inflammation can provide a proper microenvironment for tumour development, which has been known as one of the risk factors of tumorigenesis in many tumours. To investigate the tumorigenesis of FISS and screen for its potential therapeutic targets, cyclooxygenase-2 (COX-2), an inflammation-enhancing enzyme, was selected as a target for this study. In vitro experiments using FISS- and normal tissue-derived primary cells and robenacoxib, a highly selective COX-2 inhibitor, were performed. The results demonstrated that expression of COX-2 could be detected in formalin-fixed and paraffin-embedded FISS tissues and FISS-derived primary cells. Cell viability, migration and colony formation of FISS-derived primary cells were inhibited, and cell apoptosis was enhanced by robenacoxib in a dose-dependent manner. However, susceptibility to robenacoxib varied in different lines of FISS primary cells and was not completely correlated with COX-2 expression. Our results suggest that COX-2 inhibitors could be potential adjuvant therapeutics against FISSs.

猫注射部位肉瘤(FISSs)是一种高度侵袭性的恶性间充质肿瘤,起源于猫的注射部位。虽然FISS的肿瘤发生机制尚不清楚,但已有共识认为FISS与注射相关创伤和外来化学物质刺激引起的慢性炎症有关。慢性炎症可以为肿瘤的发展提供适当的微环境,这是许多肿瘤发生的危险因素之一。为了研究FISS的肿瘤发生并筛选其潜在的治疗靶点,我们选择了一种炎症增强酶环氧化酶-2 (COX-2)作为本研究的靶点。体外实验使用FISS和正常组织来源的原代细胞和robenacoxib(一种高选择性COX-2抑制剂)进行。结果表明,COX-2在福尔马林固定和石蜡包埋的FISS组织和FISS原代细胞中均可检测到表达。罗苯那昔布能抑制fiss原代细胞的活力、迁移和集落形成,并能促进细胞凋亡,且呈剂量依赖性。然而,不同细胞系的FISS原代细胞对罗苯那昔布的敏感性不同,且与COX-2的表达不完全相关。我们的研究结果表明,COX-2抑制剂可能是潜在的辅助治疗fiss。
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引用次数: 0
Protocatechuic acid inhibits LPS-induced mastitis in mice through activating the pregnane X receptor 原儿茶酸通过激活孕X受体抑制lps诱导的小鼠乳腺炎
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-16 DOI: 10.1111/jcmm.17812
Lihua Zhao, Lei Jin, Bin Yang

Mastitis refers to the inflammation in the mammary gland caused by various reasons. Protocatechuic acid (PCA) exerts anti-inflammatory effect. However, no studies have shown the protective role of PCA on mastitis. We investigated the protective effect of PCA on LPS-induced mastitis in mice and elucidated its possible mechanism. LPS-induced mastitis model was established by injection of LPS into the mammary gland. The pathology of mammary gland, MPO activity and inflammatory cytokine production were detected to evaluate the effects of PCA on mastitis. In vivo, PCA significantly attenuated LPS-induced mammary pathological changes, MPO activity, TNF-α and IL-1β production. In vitro, the production of inflammatory cytokines TNF-α and IL-1β was significantly reduced by PCA. Furthermore, LPS-induced NF-κB activation was also inhibited by PCA. In addition, PCA was found to activate pregnane X receptor (PXR) transactivation and PCA dose-dependently increased the expression of PXR downstream molecule CYP3A4. In addition, the inhibitory effect of PCA on inflammatory cytokine production was also reversed when PXR was knocked down. In conclusion, the protective effects of PCA on LPS-induced mastitis in mice through regulating PXR.

乳腺炎是指由各种原因引起的乳腺炎症。原儿茶酸(PCA)具有抗炎作用。然而,尚无研究显示PCA对乳腺炎的保护作用。我们研究了PCA对lps诱导的小鼠乳腺炎的保护作用,并探讨了其可能的机制。通过在乳腺内注射LPS建立LPS致乳腺炎模型。通过检测乳腺病理、MPO活性及炎性细胞因子的产生来评价PCA对乳腺炎的治疗作用。在体内,PCA显著减弱lps诱导的乳腺病理改变、MPO活性、TNF-α和IL-1β的产生。在体外,PCA显著降低炎症因子TNF-α和IL-1β的产生。此外,PCA还能抑制lps诱导的NF-κB活化。此外,我们还发现PCA可以激活妊娠X受体(PXR)的转激活,并且PCA可以剂量依赖性地增加PXR下游分子CYP3A4的表达。此外,当PXR被敲除时,PCA对炎症细胞因子产生的抑制作用也被逆转。综上所述,PCA通过调节PXR对lps诱导的小鼠乳腺炎有保护作用。
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引用次数: 0
Therapeutic potential of melatonin in the intervertebral disc degeneration through inhibiting the ferroptosis of nucleus pulpous cells 褪黑素通过抑制髓核细胞铁下垂对椎间盘退变的治疗潜力
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-16 DOI: 10.1111/jcmm.17818
Xinyu Dou, Yunlong Ma, Qipeng Luo, Chunyu Song, Meijuan Liu, Xiao Liu, Donglin Jia, Shuiqing Li, Xiaoguang Liu

Ferroptosis, a novel type of cell death mediated by the iron-dependent lipid peroxidation, contributes to the pathogenesis of the intervertebral disc degeneration (IDD). Increasing evidence demonstrated that melatonin (MLT) displayed the therapeutic potential to prevent the development of IDD. Current mechanistic study aims to explore whether the downregulation of ferroptosis contributes to the therapeutic capability of MLT in IDD. Current studies demonstrated that conditioned medium (CM) from the lipopolysaccharide (LPS)-stimulated macrophages caused a series of changes about IDD, including increased intracellular oxidative stress (increased reactive oxygen species and malondialdehyde levels, but decreased glutathione levels), upregulated expression of inflammation-associated factors (IL-1β, COX-2 and iNOS), increased expression of key matrix catabolic molecules (MMP-13, ADAMTS4 and ADAMTS5), reduced the expression of major matrix anabolic molecules (COL2A1 and ACAN), and increased ferroptosis (downregulated GPX4 and SLC7A11 levels, but upregulated ACSL4 and LPCAT3 levels) in nucleus pulposus (NP) cells. MLT could alleviate CM-induced NP cell injury in a dose-dependent manner. Moreover, the data substantiated that intercellular iron overload was involved in CM-induced ferroptosis in NP cells, and MLT treatment alleviated intercellular iron overload and protected NP cells against ferroptosis, and those protective effects of MLT in NP cells further attenuated with erastin and enhanced with ferrostatin-1(Fer-1). This study demonstrated that CM from the LPS-stimulated RAW264.7 macrophages promoted the NP cell injury. MLT alleviated the CM-induced NP cell injury partly through inhibiting ferroptosis. The findings support the role of ferroptosis in the pathogenesis of IDD, and suggest that MLT may serve as a potential therapeutic approach for clinical treatment of IDD.

铁下垂是一种由铁依赖性脂质过氧化介导的新型细胞死亡,与椎间盘退变(IDD)的发病机制有关。越来越多的证据表明,褪黑素(MLT)显示出预防IDD发展的治疗潜力。目前的机制研究旨在探讨铁下垂的下调是否有助于MLT治疗IDD的能力。目前的研究表明,来自脂多糖(LPS)刺激的巨噬细胞的条件培养基(CM)引起了IDD的一系列变化,包括细胞内氧化应激增加(活性氧和丙二醛水平增加,但谷胱甘肽水平降低),炎症相关因子(IL-1β, COX-2和iNOS)的表达上调,关键基质分解代谢分子(MMP-13, ADAMTS4和ADAMTS5)的表达增加。降低了主要基质合成代谢分子(COL2A1和ACAN)的表达,增加了髓核(NP)细胞的铁凋亡(下调GPX4和SLC7A11水平,上调ACSL4和LPCAT3水平)。MLT对cm诱导的NP细胞损伤具有剂量依赖性。此外,数据证实细胞间铁超载参与cm诱导的NP细胞铁凋亡,MLT处理可减轻细胞间铁超载并保护NP细胞免受铁凋亡,且MLT对NP细胞的保护作用在erastin作用下进一步减弱,在ferstat -1(fer1)作用下进一步增强。本研究表明lps刺激RAW264.7巨噬细胞产生的CM可促进NP细胞损伤。MLT减轻cm诱导的NP细胞损伤部分是通过抑制铁下垂来实现的。这些发现支持了铁下垂在IDD发病机制中的作用,并提示MLT可能作为临床治疗IDD的潜在治疗方法。
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引用次数: 3
LncRNA H19 ameliorates myocardial infarction-induced myocardial injury and maladaptive cardiac remodelling by regulating KDM3A LncRNA H19通过调节KDM3A改善心肌梗死诱导的心肌损伤和心脏重构不良
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-16 DOI: 10.1111/jcmm.17753

In Bofang Zhang et al.,1 the published article contains errors in Figures 6 and 8. The correct images are shown below. The authors confirm all results and conclusions of this article remain unchanged.

在Bofang Zhang et al.,1发表的文章中,错误见图6和图8。正确的图像如下所示。作者确认本文的所有结果和结论保持不变。
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引用次数: 1
Elevation of neutrophil-derived factors in patients after multiple trauma 多发创伤后患者中性粒细胞衍生因子的升高
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-16 DOI: 10.1111/jcmm.17786
Marie-Therese Lingitz, Gregor Wollner, Jonas Bauer, Hannes Kuehtreiber, Michael Mildner, Dragan Copic, Daniel Bormann, Martin Direder, Claus Georg Krenn, Thomas Haider, Lukas Leopold Negrin, Hendrik jan Ankersmit

Trauma represents one of the leading causes of death worldwide. Traumatic injuries elicit a dynamic inflammatory response with systemic release of inflammatory cytokines. Disbalance of this response can lead to systemic inflammatory response syndrome or compensatory anti-inflammatory response syndrome. As neutrophils play a major role in innate immune defence and are crucial in the injury-induced immunological response, we aimed to investigate systemic neutrophil-derived immunomodulators in trauma patients. Therefore, serum levels of neutrophil elastase (NE), myeloperoxidase (MPO) and citrullinated histone H3 (CitH3) were quantified in patients with injury severity scores above 15. Additionally, leukocyte, platelet, fibrinogen and CRP levels were assessed. Lastly, we analysed the association of neutrophil-derived factors with clinical severity scoring systems. Although the release of MPO, NE and CitH3 was not predictive of mortality, we found a remarkable increase in MPO and NE in trauma patients as compared with healthy controls. We also found significantly increased levels of MPO and NE on Days 1 and 5 after initial trauma in critically injured patients. Taken together, our data suggest a role for neutrophil activation in trauma. Targeting exacerbated neutrophil activation might represent a new therapeutic option for critically injured patients.

创伤是全世界死亡的主要原因之一。创伤性损伤引起全身炎症细胞因子释放的动态炎症反应。这种反应的不平衡可导致全身炎症反应综合征或代偿性抗炎反应综合征。由于中性粒细胞在先天免疫防御中起着重要作用,在损伤诱导的免疫反应中起着至关重要的作用,我们的目的是研究创伤患者全身中性粒细胞衍生的免疫调节剂。因此,在损伤严重程度评分在15分以上的患者中,对血清中性粒细胞弹性酶(NE)、髓过氧化物酶(MPO)和瓜氨酸组蛋白H3 (CitH3)水平进行量化。此外,评估白细胞、血小板、纤维蛋白原和CRP水平。最后,我们分析了中性粒细胞衍生因子与临床严重程度评分系统的关系。虽然MPO、NE和CitH3的释放不能预测死亡率,但我们发现创伤患者的MPO和NE与健康对照相比显著增加。我们还发现,危重患者在初次创伤后第1天和第5天MPO和NE水平显著升高。综上所述,我们的数据表明中性粒细胞激活在创伤中的作用。靶向加重中性粒细胞活化可能是危重损伤患者的一种新的治疗选择。
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引用次数: 0
The effect of apigenin, an aryl hydrocarbon receptor antagonist, in Phthalate-Exacerbated eosinophilic asthma model 芳烃受体拮抗剂芹菜素在邻苯二甲酸盐加重的嗜酸性哮喘模型中的作用
IF 5.3 2区 医学 Q1 Biochemistry, Genetics and Molecular Biology Pub Date : 2023-06-14 DOI: 10.1111/jcmm.17804
Seo-Hee Kim, Quang Luu Quoc, Hae-Sim Park, Yoo Seob Shin

Endocrine disrupting chemicals have been known to contribute to the aggravation of inflammatory diseases including asthma. We aimed to investigate the effects of mono-n-butyl phthalate (MnBP) which is one of the representing phthalates, and its antagonist in an eosinophilic asthma mouse model. BALB/c mice were sensitized by intraperitoneal injection of ovalbumin (OVA) with alum and followed by three nebulized OVA challenges. MnBP was administered through drinking water administration throughout the study period, and its antagonist, apigenin, was orally treated for 14 days before OVA challenges. Mice were assessed for airway hyperresponsiveness (AHR), differential cell count and type 2 cytokines in bronchoalveolar lavage fluid were measured in vivo. The expression of the aryl hydrocarbon receptor was markedly increased when MnBP was administered. MnBP treatment increased AHR, airway inflammatory cells (including eosinophils), and type 2 cytokines following OVA challenge compared to vehicle-treated mice. However, apigenin treatment reduced all asthma features, such as AHR, airway inflammation, type 2 cytokines, and the expression of the aryl hydrocarbon receptor in MnBP-augmented eosinophilic asthma. Our study suggests that MnBP exposure may increase the risk of eosinophilic inflammation, and apigenin treatment may be a potential therapy for asthma exacerbated by endocrine-disrupting chemicals.

众所周知,破坏内分泌的化学物质会加重包括哮喘在内的炎症性疾病。我们的目的是研究邻苯二甲酸单正丁酯(MnBP)及其拮抗剂在嗜酸性哮喘小鼠模型中的作用。BALB/c小鼠通过腹膜内注射含明矾的卵清蛋白(OVA)致敏,然后进行三次雾化OVA激发。在整个研究期间,MnBP通过饮用水给药,其拮抗剂芹菜素口服治疗14天 OVA挑战前几天。评估小鼠的气道高反应性(AHR),在体内测量支气管肺泡灌洗液中的差异细胞计数和2型细胞因子。当施用MnBP时,芳烃受体的表达显著增加。与载体治疗的小鼠相比,MnBP治疗增加了OVA激发后的AHR、气道炎症细胞(包括嗜酸性粒细胞)和2型细胞因子。然而,芹菜素治疗降低了所有哮喘特征,如AHR、气道炎症、2型细胞因子,以及MnBP增强的嗜酸性粒细胞性哮喘中芳烃受体的表达。我们的研究表明,MnBP暴露可能会增加嗜酸性粒细胞炎症的风险,芹菜素治疗可能是一种潜在的治疗因内分泌干扰化学物质而加剧的哮喘的方法。
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