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Retraction. 撤回。
IF 2.5 Q3 CELL BIOLOGY Pub Date : 2024-06-30 DOI: 10.33594/000000711
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引用次数: 0
Expression of Concern. 表达关切。
IF 2.5 Q3 CELL BIOLOGY Pub Date : 2024-06-30 DOI: 10.33594/000000708
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引用次数: 0
Retraction. 撤回。
IF 2.5 Q3 CELL BIOLOGY Pub Date : 2024-06-30 DOI: 10.33594/000000710
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引用次数: 0
Expression of Concern. 表达关切。
IF 2.5 Q3 CELL BIOLOGY Pub Date : 2024-06-30 DOI: 10.33594/000000709
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引用次数: 0
Cardiotoxicity Induced by Intratracheal Instillation of Diesel Exhaust Particles in Mice, and the Protective Effects of Carnosol: Suppression of Inflammation and Oxidative and Nitrosative Stress via Modulation of NF-κb/MAPKs Signaling Pathways. 气管内灌注柴油机废气颗粒对小鼠心脏的毒性及卡诺醇的保护作用:通过调节 NF-κb/MAPKs 信号通路抑制炎症、氧化和亚硝基应激。
IF 2.5 Q3 CELL BIOLOGY Pub Date : 2024-06-14 DOI: 10.33594/000000707
Nur Elena Zaaba, Sumaya Beegam, Ozaz Elzaki, Mohammad Albastaki, Majed Alhammadi, Abdallah Alsaadi, Abderrahim Nemmar

Background/aims: Inhaled particulate air pollution is associated with cardiotoxicity with underlying mechanisms including oxidative stress and inflammation. Carnosol, commonly found in rosemary and sage, is known to possess a broad range of therapeutic properties such as antioxidant, anti-inflammatory and antiapoptotic. However, its cardioprotective effects on diesel exhaust particles (DEPs)-induced toxicity have not been studied yet. Hence, we evaluated the potential ameliorative effects of carnosol on DEPs-induced heart toxicity in mice, and the underlying mechanisms involved.

Methods: Mice were intratracheally instilled with DEPs (1 mg/kg) or saline, and 1 hour prior to instillation they were given intraperitoneally either carnosol (20 mg/kg) or saline. Twenty-four hours after the DEPs instillation, multiple parameters were evaluated in the heart by enzyme-linked immunosorbent assay, colorimetric assay, Comet assay and Western blot technique.

Results: Carnosol has significantly reduced the elevation in the plasma levels of lactate hydrogenase and brain natriuretic peptide induced by DEPs. Likewise, the augmented cardiac levels of proinflammatory cytokines, lipid peroxidation, and total nitric oxide in DEPs-treated groups were significantly normalized with the treatment of carnosol. Moreover, carnosol has markedly reduced the heart mitochondrial dysfunction, as well as DNA damage and apoptosis of mice treated with DEPs. Similarly, carnosol significantly reduced the elevated expressions of phosphorylated nuclear factor-кB (NF-кB) and mitogen-activated protein kinases (MAPKs) in the hearts. Furthermore, the treatment with carnosol has restored the decrease in the expression of sirtuin-1 in the hearts of mice exposed to DEPs.

Conclusion: Carnosol significantly attenuated DEP-induced cardiotoxicity in mice by suppressing inflammation, oxidative stress, DNA damage, and apoptosis, at least partly via mechanisms involving sirtuin-1 activation and the inhibition of NF-кB and MAPKs activation.

背景/目的:吸入性微粒空气污染与心脏毒性有关,其潜在机制包括氧化应激和炎症。众所周知,迷迭香和鼠尾草中常见的卡诺醇具有广泛的治疗特性,如抗氧化、抗炎和抗细胞凋亡。然而,它对柴油机废气微粒(DEPs)诱导的毒性的心脏保护作用尚未得到研究。因此,我们评估了肌醇对柴油机废气颗粒诱发的小鼠心脏毒性的潜在改善作用及其潜在机制:方法:向小鼠气管内灌注DEPs(1毫克/千克)或生理盐水,并在灌注前1小时腹腔注射肌醇(20毫克/千克)或生理盐水。灌入DEPs 24小时后,通过酶联免疫吸附试验、比色试验、彗星试验和Western印迹技术对心脏的多项参数进行评估:结果:卡诺索能明显降低 DEPs 引起的血浆乳酸氢化酶和脑钠肽水平的升高。同样,经 DEPs 处理组的心脏促炎细胞因子、脂质过氧化物和总一氧化氮水平的升高在肌醇的作用下也明显趋于正常。此外,肌肽醇还明显减少了 DEPs 治疗组小鼠的心脏线粒体功能障碍、DNA 损伤和细胞凋亡。同样,肌醇还能明显降低心脏中磷酸化核因子-кB(NF-кB)和丝裂原活化蛋白激酶(MAPKs)的表达。此外,卡诺索尔还能恢复暴露于DEPs的小鼠心脏中sirtuin-1表达的减少:结论:卡诺索通过抑制炎症、氧化应激、DNA损伤和细胞凋亡,明显减轻了DEP诱导的小鼠心脏毒性,至少部分机制涉及sirtuin-1的激活以及NF-кB和MAPKs激活的抑制。
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引用次数: 0
Curbing Breast Cancer by Altering V-ATPase Action on F-Actin, Heterochromatin, ETV7 and mTORC2 Signaling. 通过改变 V-ATP 酶对 F-肌动蛋白、异染色质、ETV7 和 mTORC2 信号的作用抑制乳腺癌的发生
IF 2.5 Q3 CELL BIOLOGY Pub Date : 2024-06-12 DOI: 10.33594/000000706
Zeina S Khan, Fazle Hussain

Background/aims: Motivated by the vacuolar proton pump's importance in cancer, we investigate the effects of proton pump inhibition on breast cancer cell migration and proliferation, F-actin polymerization, lamin A/C, heterochromatin, and ETV7 expressions, nuclear size and shape, and AKT/mTOR signaling.

Methods: Lowly metastatic MCF7 and highly metastatic MDA-MB-231 breast cancer cells were treated with 120 nM of proton pump inhibitor Bafilomycin A1 for 24 hours. Cell migration was studied with wound- scratch assays, ATP levels with a chemiluminescent assay; cell proliferation was quantified by a cell area expansion assay. Nuclear size and shape were determined using DAPI nuclear stain and fluorescence microscopy. The levels of F-actin, lamin A/C, heterochromatin, and ETV7 were quantified using both immunocytochemistry and western blots; p-mTORC1, p-mTORC2, mTOR, p-AKT, and AKT were measured by western blots.

Results: We reveal that proton pump inhibition reduces F-actin polymerization, cell migration, proliferation, and increases heterochromatin in both lowly and highly metastatic cells. Surprisingly, Bafilomycin decreases lamin A/C in both cell lines. Inhibition has different effects on ETV7 expression in lowly and highly metastatic cells, as well as nuclear area, perimeter, and circularity. Bafilomycin also significantly decreases p-mTORC1, p-MTORC2, and MTOR expression in both cell lines, whereas it significantly decreases p-AKT in lowly metastatic cells and surprisingly significantly increases p-AKT in highly metastatic cells. Our proton pump inhibition protocol reduces V-ATPase levels (~25%) within three hours. V-ATPase levels vary in time for both control and inhibited cells, and inhibition reduces cellular ATP.

Conclusion: Proton pumps promote F-actin polymerization and decrease heterochromatin, facilitating invasion. These pumps also upregulate both mTORC1 and mTORC2, thus highlighting the relevance of vacuolar proton pumps as metastatic cancer targets.

背景/目的:鉴于空泡质子泵在癌症中的重要性,我们研究了质子泵抑制剂对乳腺癌细胞迁移和增殖、F-肌动蛋白聚合、层粘连蛋白A/C、异染色质和ETV7表达、核大小和形状以及AKT/mTOR信号转导的影响:方法:用 120 nM 的质子泵抑制剂巴佛洛霉素 A1 处理低转移性 MCF7 和高转移性 MDA-MB-231 乳腺癌细胞 24 小时。细胞迁移采用伤口划痕试验进行研究,ATP 水平采用化学发光试验进行研究;细胞增殖采用细胞面积扩大试验进行量化。使用 DAPI 核染色和荧光显微镜测定细胞核的大小和形状。通过免疫细胞化学和 Western 印迹对 F-肌动蛋白、层粘连蛋白 A/C、异染色质和 ETV7 的水平进行了量化;通过 Western 印迹对 p-mTORC1、p-mTORC2、mTOR、p-AKT 和 AKT 进行了测定:结果:我们发现,质子泵抑制剂可减少低转移细胞和高转移细胞的 F-肌动蛋白聚合、细胞迁移和增殖,并增加异染色质。令人惊讶的是,巴佛洛霉素会降低两种细胞系中的层粘连蛋白 A/C。抑制作用对低转移细胞和高转移细胞中 ETV7 的表达以及核面积、周长和圆度都有不同的影响。巴佛洛霉素还能显著降低两种细胞系中的p-mTORC1、p-MTORC2和MTOR的表达,同时显著降低低度转移细胞中的p-AKT,而令人惊讶的是能显著增加高度转移细胞中的p-AKT。我们的质子泵抑制方案可在三小时内降低 V-ATPase 的水平(约 25%)。对照细胞和受抑制细胞的 V-ATP 酶水平随时间变化,抑制会降低细胞 ATP:结论:质子泵可促进 F-肌动蛋白聚合,减少异染色质,从而促进侵袭。这些泵还能上调 mTORC1 和 mTORC2,从而突出了空泡质子泵作为转移性癌症靶点的相关性。
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引用次数: 0
Adaptive Effects of Intermittent Hypoxia Training on Oxygen-Dependent Processes as a Potential Therapeutic Strategy Tool. 间歇性缺氧训练对氧气依赖过程的适应性影响,是一种潜在的治疗策略工具。
Q3 CELL BIOLOGY Pub Date : 2024-06-10 DOI: 10.33594/000000705
Natalia Kurhaluk, Oleksandr Lukash, Piotr Kamiński, Halina Tkaczenko

Background/aims: Important benefits of intermittent hypoxic training (IHT) have emerged as an effective tool for enhancing adaptive potential in different pathological states, among which acute hypoxia dominates. Therefore, the aim of our study was to evaluate the mechanisms related to the effects of the nitric oxide system (nitrites, nitrates, carbamide, and total polyamine content) on ADP-stimulated oxygen consumption and oxidative phosphorylation in heart and liver mitochondria and biomarkers of oxidative stress in the blood, heart, and liver of rats exposed to the IHT method and acute hypoxia and treated with the amino acid L-arginine (600 mg/kg, 30 min) or the NO synthase inhibitor L-NNA (35 mg/kg, 30 min) prior to each IHT session.

Methods: We analysed the modulation of the system of oxygen-dependent processes (mitochondrial respiration with the oxygraphic method, microsomal oxidation, and lipoperoxidation processes using biochemical methods) in tissues during IHT in the formation of short-term and long-term effects (30, 60, and 180 days after the last IHT session) with simultaneous administration of L-arginine. In particular, we investigated how mitochondrial functions are modulated during intermittent hypoxia with the use of oxidation substrates (succinate or α-ketoglutarate) in bioenergetic mechanisms of cellular stability and adaptation.

Results: The IHT method is associated with a significant increase in the production of endogenous nitric oxide measured by the levels of its stable metabolite, nitrite anion, in both plasma (almost 7-fold) and erythrocytes (more than 7-fold) of rats. The intensification of nitric oxide-dependent pathways of metabolic transformations in the energy supply processes in the heart and liver, accompanied by oscillatory mechanisms of adaptation in the interval mode, causes a probable decrease in the production of urea and polyamines in plasma and liver, but not in erythrocytes. The administration of L-arginine prior to the IHT sessions increased the level of the nitrite-reducing component of the nitric oxide cycle, which persisted for up to 180 days of the experiment.

Conclusion: Thus, the efficacy of IHT and its nitrite-dependent component shown in this study is associated with the formation of long-term adaptive responses by preventing the intensification of lipoperoxidation processes in tissues due to pronounced changes in the main enzymes of antioxidant defence and stabilisation of erythrocyte membranes, which has a pronounced protective effect on the system of regulation of oxygen-dependent processes as a whole.

背景/目的:间歇性缺氧训练(IHT)作为增强不同病理状态(其中以急性缺氧为主)下适应潜能的有效工具,具有重要的益处。因此,我们的研究旨在评估一氧化氮系统(亚硝酸盐、硝酸盐、碳酰胺和多胺总含量)对心脏和肝脏线粒体中 ADP 刺激的耗氧量和氧化磷酸化以及血液中氧化应激生物标志物的影响机制、大鼠暴露于 IHT 法和急性缺氧,并在每次 IHT 前接受氨基酸 L-精氨酸(600 毫克/千克,30 分钟)或 NO 合酶抑制剂 L-NNA(35 毫克/千克,30 分钟)处理。方法我们分析了 IHT 期间组织中氧依赖过程系统的调节情况(用氧图法分析线粒体呼吸,用生化方法分析微粒体氧化和脂过氧化过程),以及同时服用 L-精氨酸后形成的短期和长期效应(最后一次 IHT 治疗后 30、60 和 180 天)。我们特别研究了间歇性缺氧期间线粒体功能是如何通过氧化底物(琥珀酸或α-酮戊二酸)在细胞稳定和适应的生物能机制中进行调节的:通过测量大鼠血浆(近 7 倍)和红细胞(超过 7 倍)中一氧化氮的稳定代谢物亚硝酸阴离子的水平,可以发现 IHT 法与内源性一氧化氮的产生显著增加有关。在心脏和肝脏的能量供应过程中,一氧化氮依赖性代谢转化途径的加强,伴随着间歇模式下的振荡适应机制,导致血浆和肝脏中尿素和多胺的产生可能减少,但红细胞中的尿素和多胺的产生没有减少。在进行间歇疗法之前服用左旋精氨酸可提高一氧化氮循环中亚硝酸盐还原成分的水平,这种作用可持续到实验结束后的 180 天:因此,本研究中显示的 IHT 及其亚硝酸盐依赖成分的功效与长期适应性反应的形成有关,它通过防止组织中的脂过氧化过程加剧,使抗氧化防御的主要酶发生明显变化,并稳定红细胞膜,这对整个氧依赖过程的调节系统具有明显的保护作用。
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引用次数: 0
Erratum. 勘误。
Q3 CELL BIOLOGY Pub Date : 2024-04-30 DOI: 10.33594/000000695
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引用次数: 0
Retraction. 撤回。
Q3 CELL BIOLOGY Pub Date : 2024-04-30 DOI: 10.33594/000000698
{"title":"Retraction.","authors":"","doi":"10.33594/000000698","DOIUrl":"https://doi.org/10.33594/000000698","url":null,"abstract":"","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"58 2","pages":"199"},"PeriodicalIF":0.0,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140907896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Erratum. 勘误。
Q3 CELL BIOLOGY Pub Date : 2024-04-30 DOI: 10.33594/000000694
{"title":"Erratum.","authors":"","doi":"10.33594/000000694","DOIUrl":"https://doi.org/10.33594/000000694","url":null,"abstract":"","PeriodicalId":9845,"journal":{"name":"Cellular Physiology and Biochemistry","volume":"58 2","pages":"193-194"},"PeriodicalIF":0.0,"publicationDate":"2024-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140907855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Cellular Physiology and Biochemistry
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