ABSTRACT
<p><b>OBJECTIVE</b>To investigate the potential role of high mobility group-1 protein (HMG-1) in the pathogenesis of sepsis-induced multiple organ dysfunction syndrome in rats.</p><p><b>METHODS</b>Using a sepsis model by cecal ligation and puncture (CLP), 80 male Wistar rats were randomly divided into four groups: normal control (n = 10), sham operation (n = 10), CLP (subdivided into 2, 6, 12, 24, 48, 72 h post-CLP, n = 60), and sodium butyrate treatment (subdivided into 12, 24 h post-CLP, n = 20). At serial time points in each group, animals were sacrificed, and blood as well as tissue samples from the liver, lung, kidney and small intestine were harvested to measure organ function parameters and HMG-1 mRNA expression by the reverse transcription polymerase chain reaction (RT-PCR) taking GAPDH as an internal standard. Also, additional experiments were performed to observe the effect of treatment with sodium butyrate on survival rate in septic rats (n = 57).</p><p><b>RESULTS</b>HMG-1 mRNA levels significantly increased in various tissues during 6 - 72 h after CLP (P < 0.05 or 0.01), and were markedly inhibited by sodium butyrate at 12 h and 24 h (P < 0.05 or 0.01). Early treatment with sodium butyrate also could markedly reduce serum alanine aminotransferase, creatinine levels at 12 h post-CLP and pulmonary myeloperoxidase activities at 24 h. Furthermore, treatment with sodium butyrate could significantly improve the 1- to 6-day survival rates in animals subjected to CLP (P < 0.05 or 0.01).</p><p><b>CONCLUSIONS</b>HMG-1 might play an important role in the development of excessive inflammatory response and subsequent multiple organ dysfunction syndrome.</p>