Inhibition of septic organ failure by teprenone-induced induction of heat shock protein

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The aim of this study is to evaluate the effect of the teprenone-induced induction of the heat shock protein (HSP) on systemic organs to inhibit induction of the septic organ failure with rats. Up to 1999, we have found that application of teprenone, a HSP inducer, induces HSP-70 in lung, kidney, liver, intestinal mucosa, and diaphragm, and that teprenone has an effect to attenuate septic systemic organ failure in rats. In 2000, we have investigated the effect of teprenone to inhibit increase in cytokines that act as septic mediators under the condition of sepsis in rats. We also investigated the effects of free radicals that play an important role to elicit septic organ failure on diaphragmatic contractility in rats. It is found that 1) the sepsis-induced diaphragmatic dysfunction was elicited by the increased septic free radicals, 2) the increase in free radical scavengers, which is also elicited by sepsis, could not completely suppress the influence of the free radicals, and 3) teprenone-induced induction of HSP-70 inhibits the production of oxygen free radicals. We also investigated the effect of sepsis and free radical scavengers on pentobarbital-induced depression of excitatory synaptic transmissions in rat hippocampal slices with field EPSPs (fEPSPs). We have found that sepsis facilitates the pentobarbital-induced depression of excitatory synaptic transmissions and the free radical scavengers suppress the influences of sepsis.