To evaluate the effect of edaravone on apoptosis in hippocampal cells in a rat model of endotoxic shock.

Thirty-six male Sprague-Dawley rats, weighing 200-250 g, aged 6 weeks, were randomly divided into 3 groups (n=12 each) using a random number table: control group (group C), endotoxic shock group (group ES), and edaravone group (group E). Lipopolysaccharide 10 mg/kg was injected via the femoral vein to establish the model of endotoxic shock in ES and E groups, while the equal volume of normal saline was given in group C. In group E, edaravone 3 mg/kg was intravenously injected immediately after establishment of the model once every 2 h until the animals were sacrificed.The equal volume of normal saline was given instead of edaravone in C and ES groups.At 6 and 12 h after administration of edaravone, 6 rats in each group were sacrificed, and the hippocampi were isolated for determination of malondialdehyde (MDA) content (using thiobarbituric acid method), tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) contents (using enzyme-linked immunosorbent assay), and cell apoptosis in hippocampal CA1 region (by TUNEL assay). The apoptotic index was calculated.

Compared with group C, the MDA, TNF-α and IL-6 contents were significantly increased at 6 and 12 h after administration of edaravone, and the apoptotic index was increased at 12 h after administration of edaravone in ES and E groups.Compared with group ES, the MDA, TNF-α and IL-6 contents were significantly decreased at 6 and 12 h after administration of edaravone, and the apoptotic index was decreased at 12 h after administration of edaravone in group E.

Edaravone can reduce apoptosis in hippocampal cells, and the mechanism is associated with the reduced oxidative stress and inflammatory responses in a rat model of endotoxic shock.

Free radical scavengers; Shock, septic; Hippocampus; Apoptosis