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Source: Free Radical Biology and Medicine

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Total 199 results found since Jan 2013.

Cigarettesmoke extract (CSE) induces transient receptor potential ankyrin 1(TRPA1)expression via activation of HIF1 αin A549 cells.
Cigarettesmoke extract (CSE) induces transient receptor potential ankyrin 1(TRPA1)expression via activation of HIF1αin A549 cells. Free Radic Biol Med. 2016 Jul 29; Authors: Nie Y, Huang C, Zhong S, Wortley MA, Luo Y, Luo W, Xie Y, Lai K, Zhong N Abstract We previously found that transient receptor potential ankyrin 1 (TRPA1) in guinea pig tracheal epithelial cells was elevated after 14 days of cigarette smoke (CS) exposure. However, the mechanism underlying CS-induced TRPA1 expression remains unknown. Here, we explored whether cigarette smoke extract (CSE) increases TRPA1 expression in A549 cells an...
Source: Free Radical Biology and Medicine - July 28, 2016 Category: Biology Authors: Nie Y, Huang C, Zhong S, Wortley MA, Luo Y, Luo W, Xie Y, Lai K, Zhong N Tags: Free Radic Biol Med Source Type: research

Endo-PDI is required for TNFα-induced angiogenesis.
Conclusion: Our study establishes Endo-PDI as a novel, important mediator of AP-1 driven gene expression and endothelial angiogenic function. PMID: 24103565 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - October 5, 2013 Category: Biology Authors: de Lucca Camargo L, Babelova A, Mieth A, Weigert A, Mooz J, Rajalingam K, Heide H, Wittig I, Rossetti Lopes L, Brandes RP Tags: Free Radic Biol Med Source Type: research

P2Y2R activation by nucleotides released from oxLDL-treated endothelial cells (ECs) mediates the interaction between ECs and immune cells through RAGE expression and reactive oxygen species production.
Abstract Lipoprotein oxidation, inflammation, and immune responses involving the vascular endothelium and immune cells contribute to the pathogenesis of atherosclerosis. In an atherosclerotic animal model, P2Y2 receptor (P2Y2R) upregulation and stimulation were previously shown to induce intimal hyperplasia and increased intimal monocyte infiltration. Thus, we investigated the role of P2Y2R in oxidized low-density lipoprotein (oxLDL)-mediated oxidative stress and the subsequent interaction between endothelial cells (ECs) and immune cells. The treatment of human ECs with oxLDL caused the rapid release of ATP (maxim...
Source: Free Radical Biology and Medicine - January 29, 2014 Category: Biology Authors: Eun SY, Park SW, Lee JH, Chang KC, Kim HJ Tags: Free Radic Biol Med Source Type: research

Intratracheal administration of mitochondrial DNA directly provokes lung inflammation through the TLR9-p38 MAPK pathway.
CONCLUSION: The intratracheal administration of mtDNA induced a local inflammatory response in the mouse lungs that depended on the interactions of mtDNA with TLR9 and may be correlated with infiltrating macrophages that could be activated by mtDNA exposure via the TLR9-p38 MAPK signal transduction pathway. PMID: 25772007 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - March 12, 2015 Category: Biology Authors: Gu X, Wu G, Yao Y, Zeng J, Shi D, Lv T, Luo L, Song Y Tags: Free Radic Biol Med Source Type: research

Endothelial deletion of mTORC1 protects against hindlimb ischemia in diabetic mice via activation of autophagy, attenuation of oxidative stress and alleviation of inflammation.
In conclusion, our present study demonstrates that endothelial mTORC1 deletion protects against hindlimb ischemic injury in diabetic mice possibly via activation of autophagy, attenuation of oxidative stress and alleviation of inflammation. Therapeutics targeting mTORC1 may therefore represents a promising strategy to rescue limb ischemia in diabetes mellitus. PMID: 28473248 [PubMed - as supplied by publisher]
Source: Free Radical Biology and Medicine - May 1, 2017 Category: Biology Authors: Fan W, Han D, Sun Z, Ma S, Gao L, Chen J, Li X, Li X, Fan M, Li C, Hu D, Wang Y, Cao F Tags: Free Radic Biol Med Source Type: research

SIRT1 Activation by Curcumin Pre-treatment Attenuates Mitochondrial Oxidative Damage Induced by Myocardial Ischemia Reperfusion Injury.
This study was designed to investigate the protective effect of Cur pre-treatment on myocardial IRI and to elucidate this potential mechanism. Isolated and in vivo rat hearts and cultured neonatal rat cardiomyocytes were subjected to IR. Prior to this procedure, the hearts or cardiomyocytes were exposed to Cur in the absence or presence of the SIRT1 inhibitor sirtinol or SIRT1 siRNA. Cur conferred a cardio-protective effect, as shown by improved post-ischemic cardiac function, decreased myocardial infarct size, decreased myocardial apoptotic index and several biochemical parameters, including the up-regulation of the anti-...
Source: Free Radical Biology and Medicine - July 20, 2013 Category: Biology Authors: Yang Y, Duan W, Lin Y, Yi W, Liang Z, Yan J, Wang N, Deng C, Zhang S, Li Y, Chen W, Yu S, Yi D, Jin Z Tags: Free Radic Biol Med Source Type: research

The glutaredoxin/S-glutathionylation axis regulates interleukin 17A-induced pro-inflammatory responses in lung epithelial cells in association with S-glutathionylation of Nuclear Factor kappa B family proteins.
In this study, we sought to determine the impacts of S-glutathionylation on IL-17A-induced NF-κB activation and expression of pro-inflammatory mediators. C10 mouse lung alveolar epithelial cells, or primary mouse tracheal epithelial cells exposed to IL-17A show rapid activation of NF-κB, and the induction of pro-inflammatory genes. Upon IL-17A exposure, sulfenic acid formation and S-glutathionylated proteins increased. Assessment of S-glutathionylation of NF-κB pathway components revealed S-glutathionylation of RelA (RelA-SSG) and inhibitory kappa B kinase alpha (IKKα-SSG) after stimulation with IL-17A. SiRNA-mediated ...
Source: Free Radical Biology and Medicine - May 6, 2014 Category: Biology Authors: Nolin JD, Tully JE, Hoffman SM, Guala AS, van der Velden JL, Poynter ME, van der Vliet A, Anathy V, Janssen-Heininger YM Tags: Free Radic Biol Med Source Type: research

Adiponectin Ameliorates Hyperglycemia-Induced Cardiac Hypertrophy and Dysfunction by Concomitantly Activating Nrf2 and Brg1.
Abstract Hyperglycemia-induced oxidative stress is implicated in the development of cardiomyopathy in diabetes that is associated with reduced adiponectin (APN) and heme oxygenase-1(HO-1). Brahma-related gene 1 (Brg1) assists nuclear factor-erythroid-2-related factor-2 (Nrf2) to activate HO-1 to increase myocardial antioxidant capacity in response to oxidative stress. We hypothesized that reduced adiponectin (APN) impairs HO-1 induction which contributes to the development of diabetic cardiomyopathy, and that supplementation of APN may ameliorate diabetic cardiomyopathy by activating HO-1 through Nrf2 and Brg1 in ...
Source: Free Radical Biology and Medicine - March 17, 2015 Category: Biology Authors: Li H, Yao W, Irwin MG, Wang T, Wang S, Zhang L, Xia Z Tags: Free Radic Biol Med Source Type: research

The Involvement of p62-Keap1-Nrf2 antioxidative signaling pathway and JNK in the protection of natural flavonoid quercetin against hepatotoxicity.
Abstract Quercetin, one of the most abundant dietary flavonoids, is reported to have protective function against various hepatotoxicants-induced hepatotoxicity. The present study aims to investigate the critical role of nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidative signaling pathway in the protection of quercetin against hepatotoxicity. Quercetin prevented the cytotoxicity induced by a variety of hepatotoxicants including clivorine (Cliv), acetaminophen (APAP), ethanol, carbon tetrachloride (CCl4), and toosendanin (TSN) in human normal liver L-02 cells. Quercetin induced the nuclear translocatio...
Source: Free Radical Biology and Medicine - April 13, 2015 Category: Biology Authors: Ji LL, Sheng YC, Zheng ZY, Shi L, Wang ZT Tags: Free Radic Biol Med Source Type: research

Angiotensin(1-7) attenuated Angiotensin II-induced hepatocyte EMT by inhibiting NOX-derived H2O2-activated NLRP3 inflammasome/IL-1 β/Smad circuit.
Angiotensin(1-7) attenuated Angiotensin II-induced hepatocyte EMT by inhibiting NOX-derived H2O2-activated NLRP3 inflammasome/IL-1β/Smad circuit. Free Radic Biol Med. 2016 Jul 18; Authors: Zhang LL, Huang S, Ma XX, Zhang WY, Wang D, Jin SY, Zhang YP, Li Y, Li X Abstract Epithelial-mesenchymal transition (EMT) is correlated with NAPDH oxidase (NOX)-derived reactive oxygen species (ROS). The ROS-induced NOD-like receptor pyrin domain containing-3 (NLRP3) inflammasome is a novel mechanism of EMT. Angiotensin II (AngII) induces EMT by regulating intracellular ROS. Nevertheless, it has not been reported w...
Source: Free Radical Biology and Medicine - July 17, 2016 Category: Biology Authors: Zhang LL, Huang S, Ma XX, Zhang WY, Wang D, Jin SY, Zhang YP, Li Y, Li X Tags: Free Radic Biol Med Source Type: research

Nrf2-induced antiapoptotic Bcl-xL protein enhances cell survival and drug resistance.
In this study, we investigated the role of Nrf2 in the regulation of antiapoptotic Bcl-xL protein and its effect on cellular apoptosis. Treatment of mouse Hepa-1 cells with the antioxidant tert-butylhydroquinone led to the induction of Bcl-xL gene expression. Promoter mutagenesis, transfection, and chromatin immunoprecipitation assays identified an ARE between nucleotides -608 and -600 in the forward strand of the proximal Bcl-xL promoter that bound to Nrf2 and led to increased Bcl-xL gene expression. In addition, short interfering RNA (siRNA) inhibition and overexpression of Nrf2 led to a respective decrease and increase ...
Source: Free Radical Biology and Medicine - December 27, 2012 Category: Biology Authors: Niture SK, Jaiswal AK Tags: Free Radic Biol Med Source Type: research

Mechanisms for cellular NO oxidation and nitrite formation in lung epithelial cells.
Abstract Airway lining fluid contains relatively high concentrations of nitrite, and arterial blood levels of nitrite are higher than venous levels, suggesting the lung epithelium may represent an important source of nitrite in vivo. To investigate whether lung epithelial cells possess the ability to convert NO to nitrite by oxidation, and the effect of oxygen reactions on nitrite formation, the NO donor DETA NONOate was incubated with or without A549 cells or primary human bronchial epithelial (HBE) cells for 24 h under normoxic (21% O2) and hypoxic (1% O2) conditions. Nitrite production was significantly increas...
Source: Free Radical Biology and Medicine - April 30, 2013 Category: Biology Authors: Zhao XJ, Wang L, Shiva S, Tejero J, Wang J, Frizzell S, Gladwin MT Tags: Free Radic Biol Med Source Type: research

Oxidative stress induces inactivation of protein phosphatase 2A, promoting proinflammatory NF-κB in aged rat kidney.
Abstract The molecular inflammation hypothesis of aging proposes that redox dysregulation causes an age-related activation of NF-κB and its signaling to upregulate various proinflammatory genes. In the present study, we focused on the inactive form of the protein phosphastase 2A (PP2A). More specifically, we aimed to define the correlation between PP2A inactivation and NF-κB activation by age-related oxidative stress. Experimentations were designed to determine the effect of oxidative stress-induced PP2A inactivation on NF-κB activity, utilizing prooxidants t-BHP and AAPH, the PTP inhibitor Na3VO4, and the PP2A...
Source: Free Radical Biology and Medicine - April 11, 2013 Category: Biology Authors: Jin Jung K, Hyun Kim D, Kyeong Lee E, Woo Song C, Pal Yu B, Young Chung H Tags: Free Radic Biol Med Source Type: research

CO-releasing molecules and increased heme oxygenase-1 induce protein S-glutathionylation to modulate NF-κB activity in endothelial cells.
Abstract Protein glutathionylation is a protective mechanism that functions in response to mild oxidative stress. Carbon monoxide (CO) can increase the ROS concentration from a low level via the inhibition of cytochrome c oxidase. We therefore hypothesized that CO would induce NF-κB-p65 glutathionylation and then show anti-inflammatory effects. In our present study, we found that CO releasing molecules suppress TNFα-induced monocyte adhesion to endothelial cells (ECs) and reduce ICAM-1 expression. Moreover, CO donors were further found to exert their inhibitory effects by blocking NF-κB-p65 nuclear translocatio...
Source: Free Radical Biology and Medicine - February 7, 2014 Category: Biology Authors: Yeh PY, Li CY, Hsieh CW, Yang YC, Yang PM, Wung BS Tags: Free Radic Biol Med Source Type: research

Upregulation of Cannabinoid Receptor-1 and Fibrotic Activation of Mouse Hepatic Stellate Cells during Schistosoma J. Infection: Role of NADPH Oxidase.
Abstract The endocannabinoid system (CS) has been implicated in the development of hepatic fibrosis such as schistosomiasis-associated liver fibrosis (SSLF). However, the mechanisms mediating the action of the CS in hepatic fibrosis is unclear. The present study hypothesized that Schistosoma J. infection upregulates cannabinoid receptor 1 (CB1) due to activation of NADPH oxidase leading to a fibrotic phenotype in hepatic stellate cells (HSCs). The SSLF model was developed by infecting mice with Schistosoma J. cercariae in the skin, and HSCs from control and infected mice were then isolated, cultured and confirmed ...
Source: Free Radical Biology and Medicine - March 18, 2014 Category: Biology Authors: Wang M, Abais JM, Meng N, Zhang Y, Ritter JK, Li PL, Tang WX Tags: Free Radic Biol Med Source Type: research