Effects of propofol on pro-inflammatory cytokines and nuclear factor kappaB during polymicrobial sepsis in rats

Nuclear factor kappa B (NF-κB) plays a central role in regulating the transcription of several genes associated with sepsis/septic shock. Therefore, the author investigated the effects of propofol on the plasma tumor necrosis factor α and interleukin 6 (TNF-α and IL-6) levels and NF-κB activation during polymicrobial sepsis in rats. Male Sprague-Dawlay rats were subjected to cecal ligation and puncture (CLP, a model of polymicrobial sepsis) or sham operation. The animals were randomly assigned into four equal groups (n = 10): sham CLP group, CLP group, PPF (propofol) I group and PPF II group. Thirty minutes before CLP, propofol (5 and 10 mg kg−1 h−1, respectively) was infused continuously through the left femoral vein cannula in PPF I group or PPF II group, CLP group and sham CLP group receiving 0.9% saline only at the rates of 5 ml kg−1 h−1. The right femoral artery was cannulated to monitor mean arterial pressure (MAP) and heart rates (HR). CLP produced progressive hypotension and a first increase followed by a decrease in HR. The plasma TNF-α and IL-6 levels and the hepatic NF-κB activation significantly increased after CLP alone. Compared with CLP group, propofol treatment reversed hypotension, slightly steadied heartbeats, and decreased the plasma TNF-α and IL-6 levels, and significantly suppressed NF-κB activation. Propofol has inhibited the hepatic NF-κB activition and the pro-inflammatory cytokine response during polymicrobial sepsis in rats.