Abstract
Galectins constitute of a soluble mammalian β-galactoside binding lectin family, which play homeostatic roles in the regulation of the cell cycle, and apoptosis, in addition to their inflammatory conditions. Galectin-3 has an important role in the regulation of various inflammatory conditions including endotoxemia, and airway inflammation. Statins, the key precursor inhibitors of 3-hydroxyl-3-methyl coenzyme A (HMG-CoA) reductase, may prevent the progression of inflammation in sepsis after prior statin treatment. Endotoxemia leads to the formation of oxidative stress parameters in proteins, carbohydrates, and DNA. In the present study, we aimed to show the effects of simvastatin on Galectin-3, and glutathione reductase (GR), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), and thiobarbituric acid reactive substances (TBARS) levels in lung tissue of rats which were treated with lipopolysaccharides (LPS) during the early phase of sepsis. Rats were divided into four groups as the control, LPS (20 mg/kg), simvastatin (20 mg/kg), and simvastatin+LPS group. Galectin-3 expression in formalin-fixed paraffin-embedded lung tissue sections was demonstrated by using the immunohistochemistry methods. There were reduced densities, and the decreased number of Galectin-3 immunoreactivities in the simvastatin+LPS group compared with the LPS group in the pneumocytes, and in the bronchial epithelium of lung tissue. In the LPS group, GR, GSH-Px, and SOD were found lower than the levels in simvastatin-treated LPS group (P<0.05, P<0.01, P<0.01 respectively) in the lung tissue. However, TBARS decreased in the simvastatin+LPS group compared with the levels in LPS group (P<0.001). Simvastatin attenuates LPS-induced oxidative acute lung inflammation, oxidative stress, and suppresses LPS-induced Galectin-3 expression in the lung tissue.
Highlights
Sepsis is defined as the development of multiple organ failure, and inflammatory responses including cellular, and metabolic changes against bacterial invasion in the host tissue [1]
We aimed to show the effects of simvastatin on the oxidative parameters: glutathione reductase (GR), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) antioxidants, thiobarbituric acid reactive substances (TBARS), and Galectin-3 in lung tissue in endotoxemia
Reduced densities and decreased number of Galectin-3 immunoreactivities in the simvastatin+LPS group were shown compared with the LPS group in pneumocytes and bronchial epithelium of lung tissue (P≤0.05) (Figures 3 and 4)
Summary
Sepsis is defined as the development of multiple organ failure, and inflammatory responses including cellular, and metabolic changes against bacterial invasion in the host tissue [1]. The lung is mostly the first affected organ in septic shock. A membrane component of Gram-negative bacteria lipopolysaccharide (LPS), which is used in experimental acute lung injury (ALI) models, and interacts with toll-like receptor 4 (TLR4), which initiates an inflammatory, and immune response. TLR4 mediates the host response to LPS by promoting the activation of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and IL-6 genes in inflammatory cells. The inflammatory cells produce cytotoxic molecules, and free radical-damaged lung tissue causes ALI [2]. The reactive oxygen species (ROS) causes tissue injury in the instances of imbalances between the ROS, and antioxidants defense mechanisms [3]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
