Burn-Induced Multiple Organ Injury and Protective Effect of Lutein in Rats
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ORIGINAL ARTICLE
Burn-Induced Multiple Organ Injury and Protective Effect of Lutein in Rats Huda O. AbuBakr,1,4 Samira H. Aljuaydi,1 Shimaa M. Abou-Zeid,2 and Amanallah El-Bahrawy3
Thermal injury may lead to multiple organ dysfunction through release of proinflammatory mediators and reactive oxygen radicals. This study investigated the effects of thermal injury on remote organs of rats and the possible protective effect of lutein. Thermal trauma was induced in the back of rats by exposing them to 90 °C bath for 10 s. Rats were sacrificed 48 h after burn, and blood samples were collected to monitor liver and kidney functions. Tissue samples from liver, kidneys, and lungs were taken for studying oxidative stress parameters, gene expressions of TNF-α and Casp-3, besides histopathological examination. Skin scald injury caused significant elevations of liver and kidney function biomarkers in the serum. In tissue samples, increments of MDA, GPx, and 8-OHdG were recorded while GSH level and the activities of CAT and SOD were suppressed. The expressions of TNF-α and caspase-3 mRNA were increased, and histopathological results revealed remote organ injury. Oral administration of lutein (250 mg/kg) resulted in amelioration of the biochemical and molecular changes induced by burn as well as the histopathological alterations. According to the findings of the present study, lutein possesses antioxidant, anti-inflammatory, and anti-apoptotic effects that protect against burn-induced damage in remote organs.
Abstract—
KEY WORDS: scald; lutein; protection; oxidative stress; TNF-α; Casp-3.
INTRODUCTION In forensic and clinical medicine, it is important to study the mechanisms of organ dysfunction resulting from burns. Severe thermal injury is caused by full-thickness burn greater than 10% of the total body surface area (TBSA) or when burn area is greater than one third of the 1
Department of Biochemistry and Chemistry of Nutrition, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt 2 Department of Forensic Medicine and Toxicology, Faculty of Veterinary Medicine, University of Sadat City, Sadat, Egypt 3 Department of Pathology, Faculty of Veterinary Medicine, University of Sadat City, Sadat, Egypt 4 To whom correspondence should be addressed at Department of Biochemistry and Chemistry of Nutrition, Faculty of Veterinary Medicine, Cairo University, Giza, 12211, Egypt. E-mail: [email protected]
TBSA [1]. Burn is a post-traumatic inflammatory disease characterized by both local effects and deleterious systemic effects in all the organ systems distant from the original wound [2, 3]. The pathophysiological mechanism of such remote organ injury in severe burn remains unclear. However, animal studies documented that reactive oxygen species (ROS) and reactive nitrogen species (RNS) mediated by elevated proinflammatory mediators released from immunocytes and necrotic cells play important roles in the development of distant organ damage [4]. It has been demonstrated that burn injury is associated with lipid peroxida
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