Amelioration of Sepsis-Induced Liver and Lung Injury by a Superoxide Dismutase Mimetic; Role of TNF-α and Caspase-3
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CLP, NO scavenger; Caspase-3; TNF-α


Oxidative stress plays an important role in the development of sepsis and its associated serious consequence leading to multiple organ failure and death. Since the liver and the lungs are among the early affected organs responsible for the mortality in sepsis, we investigated the effect of Tempol, a superoxide dismutase mimetic agent, on lung and liver injuries in a cecal ligation and puncture (CLP)-induced sepsis. Septic animals were given Tempol either before or after CLP procedure. Sepsis outcomes were assessed mainly on the liver and lungs. Separate animal groups were employed for a survival study. CLP resulted in 0% survival, while Tempol pre-or post-treatment led to a 100% and 40% survival, respectively. Administration of Tempol resulted in a significant attenuation of sepsis-induced elevation of lipid peroxidation. In the lungs and liver tissues, Tempol resulted in a significant attenuation of elevated tumor necrosis factor-α and caspase-3. Histopathological examination of the lungs and liver confirmed the protective effects of Tempol on these organs. In conclusion: Tempol acts as both prophylactic and therapeutic agent in a rat sepsis model by lowering oxidative stress, inflammatory and apoptotic signals induced by sepsis and reducing lung and liver damage induced by sepsis.

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