Protective effect of dexmedetomidine in a rat model of α-naphthylthiourea–induced acute lung injury

Hancı, Volkan; Yurdakan, Gamze; Yurtlu, Serhan; Turan, İşıl Özkoçak; Sipahi, Emine Yılmaz

doi:10.1016/j.jss.2012.02.027

Cited by 45 publications

(36 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…DEX also attenuates intestinal mucosal epithelial cell apoptosis, as observed by decreases in the apoptotic index, caspase-3 protein expression, intestinal injury and consequently rat mortality (32).…”

Section: Intestinal I/rmentioning

confidence: 94%

“…A nitric oxide synthase inhibitor, NG-nitro-L-arginine methyl ester, used prior to the administration of ANTU, significantly decreased the development of pleural effusion and the lung weight/body weight ratio (32). Thus, DEX may diminish acute N-methyl-D-aspartic acid-induced perturbation of neurotransmission (33).…”

Section: Signaling Pathwaysmentioning

confidence: 99%

“…It has also been reported that DEX reduces the expression of the pro-apoptotic protein B-cell lymphoma-associated X, as well as increasing the anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein, thereby attenuating apoptosis by inhibiting the intrinsic apoptotic cascade activation (32). The authors consider it likely that PI3K-Akt activation is one of the survival cascades activated by DEX to induce cytoprotection.…”

Section: Inflammatory Responsementioning

confidence: 99%

“…In a recent study, it was reported that the dose-dependent administration of DEX prior to ischemia, but not following it, attenuates intestinal I/R-induced intestinal injury (32). DEX also attenuates intestinal mucosal epithelial cell apoptosis, as observed by decreases in the apoptotic index, caspase-3 protein expression, intestinal injury and consequently rat mortality (32).…”

Section: Intestinal I/rmentioning

confidence: 99%

“…DEX treatment has demonstrated a potential protective benefit on lungs by preventing ANTU-induced ALI in an experimental rat model and in intensive care patients (32), and by reducing post-pneumoperitoneal I/R injury in a ventilated rat model (69). DEX-ketamine combinations mitigate pulmonary inflammatory response-induced lung injury in endotoxemic rats, and decrease lung permeability and ALI development in rats with either hemorrhagic shock or intracranial hypertension (81).…”

Section: Lung Protectionmentioning

confidence: 99%

See 4 more Smart Citations

Molecular targets and mechanism of action of dexmedetomidine in treatment of ischemia/reperfusion injury (Review)

Cai

Jia

et al. 2014

Molecular Medicine Reports

117

View full text Add to dashboard Cite

Abstract. Dexmedetomidine (DEX), a highly specific α 2 -adrenergic agonist, which exhibits anaesthetic-sparing, analgesia and sympatholytic properties. DEX modulates gene expression, channel activation, transmitter release, inflammatory processes and apoptotic and necrotic cell death. It has also been demonstrated to have protective effects in a variety of animal models of ischemia/reperfusion (I/R) injury, including the intestine, myocardial, renal, lung, cerebral and liver. The broad spectrum of biological activities associated with DEX continues to expand, and its diverse effects suggest that it may offer a novel therapeutic approach for the treatment of human diseases with I/R involvement.

show abstract

Section: Intestinal I/rmentioning

confidence: 94%

Section: Signaling Pathwaysmentioning

confidence: 99%

Section: Inflammatory Responsementioning

confidence: 99%

Section: Intestinal I/rmentioning

confidence: 99%

Section: Lung Protectionmentioning

confidence: 99%

See 3 more Smart Citations

Molecular targets and mechanism of action of dexmedetomidine in treatment of ischemia/reperfusion injury (Review)

Cai

Jia

et al. 2014

Molecular Medicine Reports

117

View full text Add to dashboard Cite

show abstract

Chrysin ameliorates ANTU‐induced pulmonary edema and pulmonary arterial hypertension via modulation of VEGF and eNOs

Wang

Zhang

2019

J Biochem & Molecular Tox

View full text Add to dashboard Cite

Alpha-naphthylthiourea (ANTU), a rodenticide induces lung toxicity. Chrysin a flavonoid possesses antioxidant, anti-inflammatory, and antihypertensive potential.The aim of this study was to evaluate the efficacy of chrysin against ANTU-induced pulmonary edema (PE) and pulmonary arterial hypertension (PAH) in laboratory rats.Sprague-Dawley rats were used to induce PE (ANTU, 10 mg/kg, ip) and PAH (ANTU, 5 mg/kg, ip, 4 weeks). Animals were treated with chrysin (10, 20, and 40 mg/kg) and various biochemical, molecular, and histological parameters were evaluated. Acute administration of ANTU induces PE revealed by significant (P < 0.05) increase in relative lung weight, pleural effusion volume, lung edema, bronchoalveolar lavage fluid cell counts, total protein, 5-hydroxytryptamine (5-HT), lactate dehydrogenase (LDH), and γ-glutamyl transferase (GGT), whereas pretreatment with chrysin (20 and 40 mg/kg, ip) significantly (P < 0.05) attenuated these ANTU-induced biochemical and histological alterations. Repeated administration of ANTU caused induction of PAH evaluated by significant (P < 0.05) alterations in electrocardiographic, hemodynamic changes, and left ventricular function, whereas chrysin (20 and 40 mg/kg, p.o.) treatment significantly (P < 0.05) attenuated these alterations. ANTU-induced hematological and serum biochemical (aspartate transaminase, alanine transaminase, LDH, and creatinine kinase MB) alterations were significantly (P < 0.05) inhibited by chrysin. It also significantly (P < 0.05) decreased elevated levels of oxido-nitrosative stress in the right ventricle (RV) and lung. Chrysin significantly (P < 0.05) attenuated downregulated endothelial nitric oxide synthase and upregulated vascular endothelial growth factor messenger RNA and protein expressions both in the RV and pulmonary artery. Chrysin inhibited ANTU-induced PE and PAH via modulation of inflammatory responses (5-HT, LDH, and GGT), oxido-nitrosative stress, and VEGF and eNOs levels.K E Y W O R D S alpha-naphthylthiourea, chrysin, eNOs, pulmonary arterial hypertension, pulmonary edema, vascular endothelial growth factor J Biochem Mol Toxicol. 2019;33:e22332.wileyonlinelibrary.com/journal/jbt

show abstract

Dexmedetomidine Suppressed the Biological Behavior of HK-2 Cells Treated with LPS by Down-Regulating ALKBH5

Zhu

2020

Inflammation

View full text Add to dashboard Cite

Protective effect of dexmedetomidine in a rat model of α-naphthylthiourea–induced acute lung injury

Cited by 45 publications

References 36 publications

Molecular targets and mechanism of action of dexmedetomidine in treatment of ischemia/reperfusion injury (Review)

Molecular targets and mechanism of action of dexmedetomidine in treatment of ischemia/reperfusion injury (Review)

Chrysin ameliorates ANTU‐induced pulmonary edema and pulmonary arterial hypertension via modulation of VEGF and eNOs

Dexmedetomidine Suppressed the Biological Behavior of HK-2 Cells Treated with LPS by Down-Regulating ALKBH5

Contact Info

Product

Resources

About