The protective effect of infliximab against carbon tetrachloride-induced acute lung injury

  • سال انتشار: 1395
  • محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 19، شماره: 6
  • کد COI اختصاصی: JR_IJBMS-19-6_015
  • زبان مقاله: انگلیسی
  • تعداد مشاهده: 195
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نویسندگان

Aysel Kurt

Recep Tayyip Erdogan University, School of Medicine, Department of Thoracic Surgery, Rize, Turkey

Levent Tumkaya

Recep Tayyip Erdogan University, School of Medicine, Department of Histology and Embryology, Rize, Turkey

Suleyman Yuce

Department of Internal Medicine, Ordu Kumru State Hospital, Ordu, Turkey

Hasan Turut

Recep Tayyip Erdogan University, School of Medicine, Department of Thoracic Surgery, Rize, Turkey

Medine Cumhur Cure

Recep Tayyip Erdogan University, School of Medicine, Department of Biochemistry, Rize, Turkey

Ibrahim Sehitoglu

Recep Tayyip Erdogan University, School of Medicine, Department of Pathology, Rize, Turkey

Yildiray Kalkan

Recep Tayyip Erdogan University, School of Medicine, Department of Histology and Embryology, Rize, Turkey

Gokhan Pusuroglu

Recep Tayyip Erdogan University, School of Medicine, Department of Internal Medicine, Rize, Turkey

Erkan Cure

Recep Tayyip Erdogan University, School of Medicine, Department of Internal Medicine, Rize, Turkey

چکیده

Objective(s): Carbon tetrachloride (CCl۴) causes pulmonary toxicity. Infliximab (Ib) is a potent inhibitor of tumor necrosis factor-alpha (TNF-α). We aimed to investigate whether Ib has a protective effect on CCl۴ induced lung injury. Materials and Methods:Rats were divided into control, CCl۴, and CCl۴+Ib groups. A single dose of ۲ ml/kg CCI۴ was administered to CCI۴ group and a single dose of ۷ mg/kg Ib was given to CCl۴+Ib group ۲۴ hr before applying CCI۴. Results:TNF-α, malondialdehyde (MDA), nitric oxide (NO) and caspase-۳ levels of the CCl۴ group were markedly higher than both the control and CCl۴+Ib groups. The CCI۴+Ib group had lower histopathological injury than the CCl۴ group. Conclusion:Ib as a strong TNF-α blocker decreases the production of proinflammatory cytokines, MDA, and oxidative stress leading to a protective effect against CCl۴ induced lung tissue injury.

کلیدواژه ها

Carbon tetrachloride, Infliximab, Nitric oxide, Pulmonary toxicity, Oxidative stress

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