Alpha-lipoic acid as a potential target for the treatment of lung injury caused by cecal ligation and puncture-induced sepsis model in rats

One of the common lethal complications of septic shock, a major cause of morbidity and mortality in patients with severe trauma and so on, is acute lung injury. alpha-Lipoic acid (ALA), with antioxidant properties, is a popular agent. Thus, we investigated the potential protective effects of ALA (20...

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Veröffentlicht in:Shock (Augusta, Ga.) Ga.), 2010-05, Vol.33 (5), p.479-484
Hauptverfasser: Cadirci, Elif, Altunkaynak, Berrin Zuhal, Halici, Zekai, Odabasoglu, Fehmi, Uyanik, M Hamidullah, Gundogdu, Cemal, Suleyman, Halis, Halici, Mesut, Albayrak, Mevlut, Unal, Bunyami
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Sprache:eng
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Zusammenfassung:One of the common lethal complications of septic shock, a major cause of morbidity and mortality in patients with severe trauma and so on, is acute lung injury. alpha-Lipoic acid (ALA), with antioxidant properties, is a popular agent. Thus, we investigated the potential protective effects of ALA (200 mg/kg) on sepsis-induced acute lung injury. Rats were exposed to cecal ligation and puncture (CLP) to induce sepsis. Rat groups were designed as (a) sham operated, (b) sham operated + ALA treated, (c) CLP applied, (d) CLP + ALA treated. Sixteen hours after CLP induction, serum samples and lung tissues were obtained for biochemical and histopathological examination. alpha-Lipoic acid decreased the serum levels of inflammatory cytokines such as TNF-alpha and IL-6, which increased after CLP. Increased activity of nuclear factor kappaB in septic lung tissues was decreased by ALA. alpha-Lipoic acid improved the decreased antioxidant activity and alleviated the increased oxidant activity, which occurred after CLP application. We can suggest that ALA showed beneficial effects by decreasing nuclear factor kappaB activation in lung tissues, resulting in decreased serum levels of TNF-alpha and IL-6, and also increasing the antioxidant capacity of the lungs.
ISSN:1073-2322
1540-0514
DOI:10.1097/SHK.0b013e3181c3cf0e