Erol Akpinar1, Zerrin Kutlu2, Duygu Kose1,3, Pelin Aydin1,4, Taha Tavaci1, Zafer Bayraktutan5, Tugba Nurcan Yuksel6, Serkan Yildirim7, Gizem Eser7, Busra Dincer8. 1. Department of Pharmacology, Faculty of Medicine, Ataturk University, Erzurum, Turkey. 2. Department of Biochemistry, Faculty of Pharmacy, Ataturk University, Erzurum, Turkey. 3. Clinical Research, Development and Design Application and Research Center, Ataturk University, Erzurum, Turkey. 4. Department of Anesthesiology and Reanimation, Educational and Research Hospital, Erzurum, Turkey. 5. Department of Biochemistry, Faculty of Medicine, Ataturk University, Erzurum, Turkey. 6. Department of Pharmacology, Faculty of Medicine, Namik Kemal University, Tekirdag, Turkey. 7. Department of Pathology, Faculty of Veterinary Medicine, Ataturk University, Erzurum, Turkey. 8. Department of Pharmacology, Faculty of Pharmacy, Erzincan Binali Yildirim University, Erzincan, Turkey.
Abstract
BACKGROUND/AIMS: Sepsis is an uncontrolled systemic infection, withcomplex pathophysiology that may result in acute lung organ damage and cause multiple organ failure. Although much research has been conducted to illuminate sepsis's complex pathophysiology, sepsis treatment protocols are limited, and sepsis remains an important cause of mortality andmorbidity in intensive care units.Various studies have shown that idebenone (IDE) possesses strong antioxidant properties, which inhibit lipid peroxidation and protect cells from oxidative damage. The present study aimed to evaluate the protective effects of IDE against lung injury in a cecal ligation and puncture (CLP)-induced sepsis rat model. METHODS: Male albino Wistar rats were used. The animals were divided into a healthy control (no treatment), CLP, IDE control (200 mg/kg), and CLP + IDE subgroups (50 mg/kg, 100 mg/kg, and 200 mg/kg), with nine rats in each group.IDE was administered 1 h after CLP induction.To evaluate the protective effects of IDE, lung tissues were collected 16 h after sepsis for biochemical, immunohistochemical staining, and histopathological examination. RESULTS: IDE significantly ameliorated sepsis-induced disturbances in oxidative stress-related factors, with its effects increasing in accordance with the dose.IDE also abolished histopathological changes in lung tissues associated with CLP.Furthermore, interleukin 1 beta (IL-1β)and tumor necrosis factor-alpha (TNF-α) immunopositivity markedly decreased in the septic rats following IDE treatment. CONCLUSIONS: IDE largely mitigated the inflammatory response in sepsis-induced lung injury by decreasing free radicals and preventing lipid peroxidation. The results suggest that IDE may represent a potential novel therapeutic drug for sepsis treatment.
BACKGROUND/AIMS: Sepsis is an uncontrolled systemic infection, withcomplex pathophysiology that may result in acute lung organ damage and cause multiple organ failure. Although much research has been conducted to illuminate sepsis's complex pathophysiology, sepsis treatment protocols are limited, and sepsis remains an important cause of mortality andmorbidity in intensive care units.Various studies have shown that idebenone (IDE) possesses strong antioxidant properties, which inhibit lipid peroxidation and protect cells from oxidative damage. The present study aimed to evaluate the protective effects of IDE against lung injury in a cecal ligation and puncture (CLP)-induced sepsis rat model. METHODS: Male albino Wistar rats were used. The animals were divided into a healthy control (no treatment), CLP, IDE control (200 mg/kg), and CLP + IDE subgroups (50 mg/kg, 100 mg/kg, and 200 mg/kg), with nine rats in each group.IDE was administered 1 h after CLP induction.To evaluate the protective effects of IDE, lung tissues were collected 16 h after sepsis for biochemical, immunohistochemical staining, and histopathological examination. RESULTS: IDE significantly ameliorated sepsis-induced disturbances in oxidative stress-related factors, with its effects increasing in accordance with the dose.IDE also abolished histopathological changes in lung tissues associated with CLP.Furthermore, interleukin 1 beta (IL-1β)and tumor necrosis factor-alpha (TNF-α) immunopositivity markedly decreased in the septic rats following IDE treatment. CONCLUSIONS: IDE largely mitigated the inflammatory response in sepsis-induced lung injury by decreasing free radicals and preventing lipid peroxidation. The results suggest that IDE may represent a potential novel therapeutic drug for sepsis treatment.