Influence of nuclear factor-kappaB inhibition on endothelin-1 induced lung edema and oxidative stress in rats

• Autorzy: Piechota A. , Goraca A.
• Języki publikacji: EN

Abstrakty

EN

The aim of the present study is to determine the effects of the BAY 11-7082, a nuclear factor-kappaB (NF-B) inhibitor, on endothelin-1 (ET-1) induced lung edema, the level of reactive oxygen species (ROS) and tumor necrosis factor alpha (TNF-) in the lungs. Experiments were carried out on adult male Wistar-Kyoto rats. The animals were divided into 4 groups: Group I: saline-treated control; Group II: saline followed by ET-1 (12.5 µg/kg b.w., i.v.); Group III: BAY 11-7082 (10 mg/kg b.w., i.v.) administered one hour before saline; Group IV: BAY 11-7082 (10 mg/kg b.w., i.v.) administered 1 hour before ET-1 (12.5 µg/kg b.w., i.v.). Injection of ET-1 alone showed a significant (P<0.001) increase in thiobarbituric acid reactive substances (TBARS) and hydrogen peroxide (H2O2) level as well as a decrease (P<0.01) in GSH level and GSH/GSSG ratio (P<0.02). BAY 11-7082 significantly decreased TBARS (P<0.01) and H2O2 (P<0.05) level as well as improved the redox status (P<0.02) in the lungs. BAY 11-7082 also prevented ET-1 induced lung edema (P<0.05). The concentration of TNF- (P<0.02) and p65 subunit of NF-B signaling compound (P<0.001) was increased in the presence of ET-1, while BAY 11-7082 decreased both TNF- level (P<0.05) and p65 subunit concentration (P<0.01). Our results indicate that BAY 11-7082 plays a protective role in ET-1 induced oxidative lung injury. It successfully prevents lung edema as well as ROS and TNF- overproduction. Our results also highlight the important role of the NF-B pathway in ET-1 induced lung injury and ROS overproduction.

Słowa kluczowe

EN

nuclear factor-kappaB; endothelin-1; lung oedema; oxidative stress; reactive oxygen species; tumour necrosis factor-alpha; glutathione; epithelial cell; macrophage; vascular endothelial cell; rat

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2011
• Tom: 62
• Numer: 2
• Opis fizyczny: p.183-188,fig.,ref.

Twórcy

autor

Piechota A.

• Experimental and Clinical Physiology, Department of Cardiovascular Physiology, 6/8 Mazowiecka Street, 92-215 Lodz, Poland

autor

Goraca A.