Abstract
Sepsis, a systemic inflammatory disease developed after an infectious insult and remains the major cause of death in intensive care units. The aim of this study was to examine the protective effect of the ethanolic extract of Ruta chalepensis L. (ERC) against oxidative stress and liver-kidney functions in cecal and ligation puncture (CLP) rats. In vitro, the results showed that ERC rich in phenolic compounds possessed important antioxidant activity. In vivo, CLP-induced oxidative stress evidenced by the increase of the TBARS and decrease in the enzymatic antioxidants (SOD, CAT, GPX) in liver and kidney. Moreover, CLP induced liver-kidney toxicities showed by an increase in the ALT, AST, PAL, LDH, BUN and creatinine in the plasma. However, the administration of ERC to CLP-rats prevents all these disorders. Positive action of ERC was confirmed by histo-pathological examination. Therefore this study suggests that ERC could be a potential therapeutic agent for sepsis treatment.
Highlights
Sepsis presents a systemic inflammation disease related to an infectious insult from agents such as bacteria, pathogenic fungi, yeasts and viruses
Several experimental studies have shown that cecal and ligation puncture (CLP) causes the inoculation of colonic content into the peritoneal cavity and results in episodic bacteremia and systemic changes such as hyperpyrexia, leukocytosis and tachycardia
Oxidative stress mediated by oxygen-derived free radicals which include hydrogen peroxide and hydroxyl radicals is an important cause of cell membrane damage
Summary
Sepsis presents a systemic inflammation disease related to an infectious insult from agents such as bacteria, pathogenic fungi, yeasts and viruses. Sepsis generally occurs in immunocompromised patients, the elderly, or patients undergoing procedures in which significant bacterial contamination may occur [4]. Sepsis is associated with heightened oxidative stress [5]. Various studies have shown that sepsis is associated with an increased oxygen free radicals formation including hydrogen peroxide (H2O2), superoxide anions (O2-) and hydroxyl radicals OH and a decreased antioxidant potential such as superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) [6]. The homeostatic balance normally present in cells between radical formation and protection by antioxidant defenses system is disturbed and subsequently leads to oxidative stress [7]. The generation of oxygen free radicals might be enhanced, leading to membrane damage, LPO, mitochondrial damage and initiation or aggravation of diverse pathological states [8,9]. The pro-inflammatory properties of ROS include endothelial damage, chemotactic factors formation, neutrophils recruitment, lipid peroxidation, DNA damage, tumor necrosis factor-alpha (TNF-α) and interleukin-1-beta (IL-1β) release and peroxynitrite formation [1]
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