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https://www.readbyqxmd.com/read/27912883/miltirone-protects-human-ea-hy926-endothelial-cells-from-oxidized-low-density-lipoprotein-derived-oxidative-stress-via-a-heme-oxygenase-1-and-mapk-nrf2-dependent-pathway
#1
Liu Zhang, Hui Zhang, Xueyan Li, Bingjie Jia, Yuyu Yang, Ping Zhou, Ping Li, Jun Chen
BACKGROUND: Oxidized low-density lipoprotein (ox-LDL) is an underlying cause of endothelial dysfunction, which is an early event in the pathogenesis of atherosclerosis. In our previous study, we established an ARE-driven luciferase reporter system and screened out several potential Nrf2 activators from Salvia miltiorrhiza Bunge. PURPOSE: Since miltirone showed the most potent ARE-driven luciferase activity, the aim of this study was to test the protective role of miltirone against oxidative stress in endothelial cell and to investigate the underlying mechanistic signaling pathways...
December 15, 2016: Phytomedicine: International Journal of Phytotherapy and Phytopharmacology
https://www.readbyqxmd.com/read/27912197/rac1-nadph-oxidase-signaling-promotes-cd36-activation-under-glucotoxic-conditions-in-pancreatic-beta-cells
#2
Suma Elumalai, Udayakumar Karunakaran, In Kyu Lee, Jun Sung Moon, Kyu Chang Won
We recently reported that cluster determinant 36 (CD36), a fatty acid transporter, plays a pivotal role in glucotoxicity-induced β-cell dysfunction. However, little is known about how glucotoxicity influences CD36 expression. Emerging evidence suggests that the small GTPase Rac1 is involved in the pathogenesis of beta cell dysfunction in type 2 diabetes (T2D). The primary objective of the current study was to determine the role of Rac1 in CD36 activation and its impact on β-cell dysfunction in diabetes mellitus...
November 23, 2016: Redox Biology
https://www.readbyqxmd.com/read/27912149/didymin-ameliorates-hepatic-injury-through-inhibition-of-mapk-and-nf-%C3%AE%C2%BAb-pathways-by-up-regulating-rkip-expression
#3
Quanfang Huang, Facheng Bai, Jinlan Nie, Shengjuan Lu, Chunyuang Lu, Xunshuai Zhu, Lang Zhuo, Xing Lin
A flavone was isolated from Origanum vulgare and identified as didymin (O. vulgare didymin, OVD). The protective effect and mechanism of OVD on acute liver injury was then assessed in vivo and in vitro. Our results showed that OVD significantly alleviated CCl4-induced liver injury in mice and markedly decreased serum ALT and AST activities. OVD treatment significantly reduced CYP2E1 activity, lipid peroxidation level, ROS generation, NO production and pro-inflammatory cytokines (such as TNF-α, IL-6 and IL-1β) in liver tissues and RAW 264...
November 29, 2016: International Immunopharmacology
https://www.readbyqxmd.com/read/27912102/toyocamycin-induces-apoptosis-via-the-crosstalk-between-reactive-oxygen-species-and-p38-erk-mapks-signaling-pathway-in-human-prostate-cancer-pc-3-cells
#4
Sul-Gi Park, Sang-Hun Kim, Kwang-Youn Kim, Sun-Nyoung Yu, Hyeun-Deok Choi, Young-Wook Kim, Hyo-Won Nam, Young-Kyo Seo, Soon-Cheol Ahn
BACKGROUND: Toyocamycin, an antibiotic agent isolated from Streptomyces species, has been shown to have anticancer and chemopreventive effects on various cancer cells. Until now, Toyocamycin-induced apoptosis has not been reported to be involved in the regulation between mitogen-activated protein kinases (MAPKs) and reactive oxygen species (ROS) production. METHODS: Cell viability assay, western blot, cell-cycle arrest, annexin V/propidium iodide assay, reactive oxygen species (ROS) production, mitochondrial membrane potential and intracellular Ca(2+) flux were assayed...
October 24, 2016: Pharmacological Reports: PR
https://www.readbyqxmd.com/read/27911877/icariside-ii-activates-egfr-akt-nrf2-signaling-and-protects-osteoblasts-from-dexamethasone
#5
Weidong Liu, Li Mao, Feng Ji, Fengli Chen, Shouguo Wang, Yue Xie
The potential effect of icariside II on dexamethasone-induced osteoblast cell damages was evaluated here. In MC3T3-E1 osteoblastic cells and the primary murine osteoblasts, co-treatment with icariside II dramatically attenuated dexamethasone- induced cell death and apoptosis. Icariside II activated Akt signaling, which is required for its actions in osteoblasts. Akt inhibitors (LY294002, perifosine and MK-2206) almost abolished icariside II-induced osteoblast cytoprotection against dexamethasone. Further studies showed that icariside II activated Nrf2 signaling, downstream of Akt, to inhibit dexamethasone-induced reactive oxygen species (ROS) production in MC3T3-E1 cells and primary osteoblasts...
December 1, 2016: Oncotarget
https://www.readbyqxmd.com/read/27911703/understanding-and-preventing-mitochondrial-oxidative-damage
#6
REVIEW
Michael P Murphy
Mitochondrial oxidative damage has long been known to contribute to damage in conditions such as ischaemia-reperfusion (IR) injury in heart attack. Over the past years, we have developed a series of mitochondria-targeted compounds designed to ameliorate or determine how this damage occurs. I will outline some of this work, from MitoQ to the mitochondria-targeted S-nitrosating agent, called MitoSNO, that we showed was effective in preventing reactive oxygen species (ROS) formation in IR injury with therapeutic implications...
October 15, 2016: Biochemical Society Transactions
https://www.readbyqxmd.com/read/27910952/protective-effects-of-ginsenoside-rg1-on-intestinal-ischemia-reperfusion-injury-induced-oxidative-stress-and-apoptosis-via-activation-of-the-wnt-%C3%AE-catenin-pathway
#7
Guo Zu, Jing Guo, Ningwei Che, Tingting Zhou, Xiangwen Zhang
Ginsenoside Rg1 (Rg1) is one of the major bioactive ingredients in Panax ginseng, and it attenuates inflammation and apoptosis. The aims of our study were to explore the potential of Rg1 for the treatment of intestinal I/R injury and to determine whether the protective effects of Rg1 were exerted through the Wnt/β-catenin signaling pathway. In this study, Rg1 treatment ameliorated inflammatory factors, ROS and apoptosis that were induced by intestinal I/R injury. Cell viability was increased and cell apoptosis was decreased with Rg1 pretreatment following hypoxia/reoxygenation (H/R) in the in vitro study...
December 2, 2016: Scientific Reports
https://www.readbyqxmd.com/read/27909046/capping-protein-modulates-actin-remodeling-in-response-to-ros-during-plant-innate-immunity
#8
Jiejie Li, Lingyan Cao, Christopher J Staiger
Plants perceive microbe-associated molecular patterns (MAMPs) and damage-associated molecular patterns (DAMPs) to activate innate immune signaling events, such as bursts of reactive oxygen species (ROS). The actin cytoskeleton remodels during the first five minutes of innate immune signaling in Arabidopsis epidermal cells; however, the immune signals that impinge on actin cytoskeleton and its response regulators remain largely unknown. Here, we demonstrate that rapid actin remodeling upon elicitation with diverse MAMPs and DAMPs represents a conserved plant immune response...
December 1, 2016: Plant Physiology
https://www.readbyqxmd.com/read/27908781/heme-oxygenase-1-metabolite-biliverdin-not-iron-inhibits-porcine-reproductive-and-respiratory-syndrome-virus-replication
#9
Angke Zhang, Hong Duan, Na Li, Lijuan Zhao, Fengxing Pu, Baicheng Huang, Chunyan Wu, Yuchen Nan, Taofeng Du, Yang Mu, Qin Zhao, Yani Sun, Gaiping Zhang, Julian A Hiscox, En-Min Zhou, Shuqi Xiao
Porcinereproductiveandrespiratorysyndromevirus (PRRSV) causes significant economic losses to the pork industry worldwide. Previously, we demonstrated that heme oxygenase-1 (HO-1) interferes with PRRSV replication. To elucidate the mechanisms involved, here we assess whether the HO-1 downstream metabolites biliverdin (BV) and/or iron mediate the HO-1 antiviral effect. We demonstrate a BV concentration-dependent suppression of PRRSV replication and show that virions are not directly inactivated by BV. Additionally, BV or N-acetyl cysteine (NAC) significantly reduced reactive oxygen species (ROS) in PRRSV-infected MARC-145 cells; however, because NAC did not reduce viral load, the BV antiviral effect is independent of decreased ROS levels...
November 28, 2016: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/27908723/oxidation-inhibits-pth-receptor-signaling-and-trafficking
#10
Juan A Ardura, Verónica Alonso, Pedro Esbrit, Peter A Friedman
Reactive Oxygen Species (ROS) increase during aging, potentially affecting many tissues including brain, heart, and bone. ROS alter signaling pathways and constitute potential therapeutic targets to limit oxidative damaging effects in aging-associated diseases. Parathyroid hormone receptors (PTHR) are widely expressed and PTH is the only anabolic therapy for osteoporosis. The effects of oxidative stress on PTHR signaling and trafficking have not been elucidated. Here, we used Fluorescence Resonance Energy Transfer (FRET)-based cAMP, ERK, and calcium fluorescent biosensors to analyze the effects of ROS on PTHR signaling and trafficking by live-cell imaging...
November 28, 2016: Biochemical and Biophysical Research Communications
https://www.readbyqxmd.com/read/27908414/licl-regulates-mitochondrial-biogenesis-during-megakaryocyte-development
#11
Ram Babu Undi, Usha Gutti, Ravi Kumar Gutti
JAK-STAT, PI3K-AKT and MAPK signaling pathways are involved in platelet production process. Although wnt signaling has been reported in the biogenesis of platelets, but its role in megakaryocyte development is not well studied. We used an inducible canonical wnt signaling system that utilizes LiCl (GSK-3β inhibitor). LiCl could activate wnt signaling pathway along with maturation of megakaryocytes. Mitochondrial staining showed an increase in mitochondrial mass upon induction with LiCl. Also, mitochondrial markers PGC-1α and TFAM were up regulated with increase in mitochondrial DNA content...
January 2017: Journal of Trace Elements in Medicine and Biology
https://www.readbyqxmd.com/read/27907115/brucella-melitensis-16m-regulates-the-effect-of-air-domain-on-inflammatory-factors-autophagy-and-apoptosis-in-mouse-macrophage-through-the-ros-signaling-pathway
#12
Tiansen Li, Yafang Xu, Laizhen Liu, Meiling Huang, Zhen Wang, Zhixia Tong, Hui Zhang, Fei Guo, Chuangfu Chen
Brucellosis is a highly contagious zoonosis caused by Brucella. Brucella can invade and persist inside host cells, which results in chronic infection. We constructed AIR interference and overexpression lentiviruses to acquire AIR interference, overexpression, and rescue stable expression cell lines. We also established a Brucella melitensis 16M-infected macrophage model, which was treated with either the vehicle control or NAC (ROS scavenger N-acetylcysteine (NAC) for 0, 3, 6, 12, and 24 h. Confocal laser microscopy, transmission electron microscopy, fluorescence quantitative PCR, flow cytometry, ELISA, and Western blot were used to detect inflammation, cell autophagy and apoptosis-related protein expression levels, ROS levels, and the distribution of mitochondria...
2016: PloS One
https://www.readbyqxmd.com/read/27907040/the-role-of-reactive-oxygen-species-in-%C3%AE-adrenergic-signaling-in-cardiomyocytes-from-mice-with-the-metabolic-syndrome
#13
Monica Llano-Diez, Jon Sinclair, Takashi Yamada, Mei Zong, Jeremy Fauconnier, Shi-Jin Zhang, Abram Katz, Kent Jardemark, Håkan Westerblad, Daniel C Andersson, Johanna T Lanner
The metabolic syndrome is associated with prolonged stress and hyperactivity of the sympathetic nervous system and afflicted subjects are prone to develop cardiovascular disease. Under normal conditions, the cardiomyocyte response to acute β-adrenergic stimulation partly depends on increased production of reactive oxygen species (ROS). Here we investigated the interplay between beta-adrenergic signaling, ROS and cardiac contractility using freshly isolated cardiomyocytes and whole hearts from two mouse models with the metabolic syndrome (high-fat diet and ob/ob mice)...
2016: PloS One
https://www.readbyqxmd.com/read/27907022/nicotine-induces-podocyte-apoptosis-through-increasing-oxidative-stress
#14
Xiqian Lan, Rivka Lederman, Judith M Eng, Seyedeh Shadafarin Marashi Shoshtari, Moin A Saleem, Ashwani Malhotra, Pravin C Singhal
BACKGROUND: Cigarette smoking plays an important role in the progression of chronic kidney disease (CKD). Nicotine, one of the major components of cigarette smoking, has been demonstrated to increase proliferation of renal mesangial cells. In this study, we examined the effect of nicotine on podocyte injury. METHODS: To determine the expression of nicotinic acetylcholine receptors (nAChR subunits) in podocytes, cDNAs and cell lysate of cultured human podocytes were used for the expression of nAChR mRNAs and proteins, respectively; and mouse renal cortical sections were subjected to immunofluorescant staining...
2016: PloS One
https://www.readbyqxmd.com/read/27906752/recent-developments-in-emerging-therapeutic-targets-of-osteoarthritis
#15
Margaret Man-Ger Sun, Frank Beier, Michael A Pest
PURPOSE OF REVIEW: Despite the tremendous individual suffering and socioeconomic burden caused by osteoarthritis, there are currently no effective disease-modifying treatment options. This is in part because of our incomplete understanding of osteoarthritis disease mechanism. This review summarizes recent developments in therapeutic targets identified from surgical animal models of osteoarthritis that provide novel insight into osteoarthritis pathology and possess potential for progression into preclinical studies...
January 2017: Current Opinion in Rheumatology
https://www.readbyqxmd.com/read/27904889/reactive-oxygen-species-in-bcr-abl1-expressing-cells-relevance-to-chronic-myeloid-leukemia
#16
Joanna Antoszewska-Smith, Elzbieta Pawlowska, Janusz Blasiak
Chronic myeloid leukemia (CML) results from the t(9;22) reciprocal chromosomal translocation producing the BCR-ABL1 gene, conferring growth and proliferation advantages in the CML cells. CML progresses from chronic, often syndrome-free, to blast phase, fatal if not treated. Although the involvement of BCR-ABL1 in some signaling pathways is considered as the cause of CML, the mechanisms resulting in its progression are not completely known. However, BCR-ABL1 stimulates the production of reactive oxygen species (ROS), which levels increase with CML progression and induce BCR-ABL1 self-mutagenesis...
December 1, 2016: Acta Biochimica Polonica
https://www.readbyqxmd.com/read/27904687/high-fructose-causes-cardiac-hypertrophy-via-mitochondrial-signaling-pathway
#17
Yan-Bo Zhang, Yan-Hai Meng, Shuo Chang, Rong-Yuan Zhang, Chen Shi
High fructose diet can cause cardiac hypertrophy and oxidative stress is a key mediator for myocardial hypertrophy. Disruption of cystic fibrosis transmembrane conductance regulator (CFTR) leads to oxidative stress. This study aims to reveal mitochondrial oxidative stress-related signaling pathway in high fructose-induced cardiac hypertrophy. Mice were fed high fructose to develop cardiac hypertrophy. Fructose and H2O2 were used to induce cardiomyocyte hypertrophy in vitro. Mitochondria-targeted antioxidant SkQ1 was applied to investigate the possible role of mitochondrial reactive oxygen species (ROS)...
2016: American Journal of Translational Research
https://www.readbyqxmd.com/read/27903972/gdf15-contributes-to-radioresistance-and-cancer-stemness-of-head-and-neck-cancer-by-regulating-cellular-reactive-oxygen-species-via-a-smad-associated-signaling-pathway
#18
Yan-Liang Li, Joseph T Chang, Li-Yu Lee, Kang-Hsing Fan, Ya-Ching Lu, Yi-Chen Li, Chang-Hsu Chiang, Guo-Rung You, Hsin-Ying Chen, Ann-Joy Cheng
Radiotherapy is an integral part for the treatment of head and neck cancer (HNC), while radioresistance is a major cause leads to treatment failure. GDF15, a member of the TGF-β superfamily, is hypothesized to participate in various types of homeostasis. However, the potential role of this molecule in regulation of radiosensitivity remains unclear. In this study, we demonstrated that GDF15 contributed to radioresistance of HNC, as determined by both gain- and lost-of-functional experiments. These results were achieved by the induction of mitochondrial membrane potential and suppression of intracellular reactive oxygen species (ROS)...
November 26, 2016: Oncotarget
https://www.readbyqxmd.com/read/27903582/threshold-levels-of-extracellular-l-arginine-that-trigger-nos-mediated-ros-rns-production-in-cardiac-ventricular-myocytes
#19
Jayalakshmi Ramachandran, R Daniel Peluffo
L-arginine (L-Arg) is the substrate for nitric oxide synthase (NOS) to produce nitric oxide (NO), a signaling molecule that is key in cardiovascular physiology and pathology. In cardiac myocytes, L-Arg is incorporated from the circulation through the functioning of system-y(+) cationic amino acid transporters. Depletion of L-Arg leads to NOS uncoupling, with O2 rather than L-Arg as terminal electron acceptor, resulting in superoxide formation. The reactive oxygen species (ROS) superoxide (O2•(-)), combined with NO, may lead to the production of the reactive nitrogen species (RNS) peroxynitrite (ONOO-), which is recognized as a major contributor to myocardial depression...
November 30, 2016: American Journal of Physiology. Cell Physiology
https://www.readbyqxmd.com/read/27903425/activation-of-akt-and-jnk-nrf2-nqo1-pathway-contributes-to-the-protective-effect-of-coptisine-against-aaph-induced-oxidative-stress
#20
Yin-Ran Hu, Hang Ma, Zong-Yao Zou, Kai He, Yu-Bo Xiao, Yue Wang, Min Feng, Xiao-Li Ye, Xue-Gang Li
Coptisine (COP) is one of the main active constituents of Coptidis Rhizoma. Previous studies have clarified that COP possesses antioxidant activity, but its defensive effects against pathological characteristics accompanied by oxidative damage in animal models and antioxidant mechanism are still unclear. Therefore, our purpose was to confirm the antioxidant activity of COP and explore its mechanism of action. We first detected the effects of COP on intracellular reactive oxygen species (ROS), heart beating rate, lipid peroxidation and cell death in zebrafish model with AAPH-induced oxidative stress...
November 27, 2016: Biomedicine & Pharmacotherapy, Biomédecine & Pharmacothérapie
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