Treatment with N-methyl-d-aspartate receptor antagonist (MK-801) protects against oxidative stress in lipopolysaccharide-induced acute lung injury in the rat

Cunha, Aline Andrea da; Nunes, Fernanda Bordignon; Lunardelli, Adroaldo; Pauli, Vânia; Amaral, Robson Henrich; Oliveira, Luciana Mello de; Saciura, Vasyl Custódio; Silva, Gabriela Lucas da; Pires, Marçal; Donadio, Márcio Vinı́cius Fagundes; Melo, Denizar Alberto da Silva; Dal‐Pizzol, Felipe; Moreira, José Cláudio Fonseca; Behr, Guilherme Antônio; Reichel, Carlos Luiz; Rosa, José Luís; Oliveira, Jarbas Rodrigues de

doi:10.1016/j.intimp.2011.01.016

Cited by 31 publications

(12 citation statements)

References 50 publications

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“…Interestingly, all of these structures can trigger the activation of inflammatory cytokine expression by Toll-like receptor (TLR)-dependent pathways (25), e.g., TLR4 (10,47) and TLR2 (6,38). Some studies have revealed that LPS could induce the production of ROS in some organs, such as lung and liver (8,51), in which ROS are important to the pathogenesis of organ damage (52).…”

Section: Discussionmentioning

confidence: 99%

Reactive Oxygen Species-Triggered Trophoblast Apoptosis Is Initiated by Endoplasmic Reticulum Stress via Activation of Caspase-12, CHOP, and the JNK Pathway in Toxoplasma gondii Infection in Mice

Liu

Zhang

et al. 2012

Infect Immun

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dToxoplasma gondii infection in pregnant women may result in abortion or in fetal teratogenesis; however, the underlying mechanisms are still unclear. In this paper, based on a murine model, we showed that maternal infection with RH strain T. gondii tachyzoites induced elevated production of reactive oxygen species (ROS), local oxidative stress, and subsequent apoptosis of placental trophoblasts. PCR array analysis of 84 oxidative stress-related genes demonstrated that 27 genes were upregulated at least 2-fold and that 9 genes were downregulated at least 2-fold in the T. gondii infection group compared with levels in the control group. The expression of NADPH oxidase 1 (Nox1) and glutathione peroxidase 6 (Gpx6) increased significantly, about 25-fold. The levels of malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG) increased significantly with T. gondii infection, and levels of glutathione (GSH) decreased rapidly. T. gondii infection increased the early expression of endoplasmic reticulum stress (ERS) markers, followed by cleavage of caspase-12, activation of ASK1/JNK, and increased apoptosis of trophoblasts, both in vivo and in vitro. The apoptosis of trophoblasts, the activation of caspase-12 and the ASK1/JNK pathway, and the production of peroxides were dramatically inhibited by pretreatment with N-acetylcysteine (NAC). The upregulation of Nox1 was contact dependent and preceded the increase in levels of ERS markers and the activation of the proapoptosis cascade. Thus, we concluded that apoptosis in placental trophoblasts was initiated predominantly by ROS-mediated ERS via activation of caspase-12, CHOP, and the JNK pathway in acute T. gondii infection. Elevated ROS production is the central event in T. gondiiinduced apoptosis of placental trophoblasts.

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Section: Discussionmentioning

confidence: 99%

Reactive Oxygen Species-Triggered Trophoblast Apoptosis Is Initiated by Endoplasmic Reticulum Stress via Activation of Caspase-12, CHOP, and the JNK Pathway in Toxoplasma gondii Infection in Mice

Liu

Zhang

et al. 2012

Infect Immun

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“…The rat model of LPS-induced lung injury used in the present study was described in detail in previous reports 2-4. In all groups, anesthesia was induced with 50 mg/kg pentobarbital sodium administered intraperitoneally and maintained with 12 mg kg -1 h -1 pentobarbital sodium via the left jugular vein; neuromuscular blockage was achieved by intravenous administration of 0.4 mg kg -1 h -1 pipecuronium bromide (Gedeon Richter Ltd., Hungary).…”

Section: Methodsmentioning

confidence: 99%

“…Intratracheal instillation of lipopolysaccharide (LPS) in the rat is a well-characterized model 2-4 of ALI, which in many important aspects closely resembles the clinical presentation of ALI and ARDS 5-7.…”

Section: Introductionmentioning

confidence: 99%

Propofol exerts anti-inflammatory effects in rats with lipopolysaccharide-induced acute lung injury by inhibition of CD14 and TLR4 expression

Zhang

et al. 2013

Braz J Med Biol Res

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We investigated the effect of propofol (Prop) administration (10 mg kg-1 h-1, intravenously) on lipopolysaccharide (LPS)-induced acute lung injury and its effect on cluster of differentiation (CD) 14 and Toll-like receptor (TLR) 4 expression in lung tissue of anesthetized, ventilated rats. Twenty-four male Wistar rats were randomly divided into three groups of 8 rats each: control, LPS, and LPS+Prop. Lung injury was assayed via blood gas analysis and lung histology, and tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) levels were determined in bronchoalveolar lavage fluid using ELISA. Real-time polymerase chain reaction was used to detect CD14 and TLR4 mRNA levels, and CD14 and TLR4 protein expression was determined by Western blot. The pathological scores were 1.2 ± 0.9, 3.3 ± 1.1, and 1.9 ± 1.0 for the control, LPS, and LPS+Prop groups, respectively, with statistically significant differences between control and LPS groups (P < 0.05) and between LPS and LPS+Prop groups (P < 0.05). The administration of LPS resulted in a significant increase in TNF-α and IL-1β levels, 7- and 3.5-fold, respectively (P < 0.05), while treatment with propofol partially blunted the secretion of both cytokines (P < 0.05). CD14 and TLR4 mRNA levels were increased in the LPS group (1.48 ± 0.05 and 1.26 ± 0.03, respectively) compared to the control group (1.00 ± 0.20 and 1.00 ± 0.02, respectively; P < 0.05), while propofol treatment blunted this effect (1.16 ± 0.05 and 1.12 ± 0.05, respectively; P < 0.05). Both CD14 and TLR4 protein levels were elevated in the LPS group compared to the control group (P < 0.05), while propofol treatment partially decreased the expression of CD14 and TLR4 protein versus LPS alone (P < 0.05). Our study indicates that propofol prevents lung injury, most likely by inhibition of CD14 and TLR4 expression.

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“…Free radicals, such as superoxide (O 2− ), hydroxyl radicals (•OH) and peroxynitrite (ONOO − ), are all important mediators of LPS-induced ALI [2,[8][9][10][11]. Treatment with antioxidants such as N-acetylcysteine, taurine, edaravone and N-methyl-D-aspartate receptor antagonist has been proved to be effective in ameliorating the LPS-induced ALI [12][13][14][15].…”

Section: Introductionmentioning

confidence: 99%

Hydrogen inhalation ameliorates lipopolysaccharide-induced acute lung injury in mice

Qiu

Tang

et al. 2011

International Immunopharmacology

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Treatment with N-methyl-d-aspartate receptor antagonist (MK-801) protects against oxidative stress in lipopolysaccharide-induced acute lung injury in the rat

Cited by 31 publications

References 50 publications

Reactive Oxygen Species-Triggered Trophoblast Apoptosis Is Initiated by Endoplasmic Reticulum Stress via Activation of Caspase-12, CHOP, and the JNK Pathway in Toxoplasma gondii Infection in Mice

Reactive Oxygen Species-Triggered Trophoblast Apoptosis Is Initiated by Endoplasmic Reticulum Stress via Activation of Caspase-12, CHOP, and the JNK Pathway in Toxoplasma gondii Infection in Mice

Propofol exerts anti-inflammatory effects in rats with lipopolysaccharide-induced acute lung injury by inhibition of CD14 and TLR4 expression

Hydrogen inhalation ameliorates lipopolysaccharide-induced acute lung injury in mice

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