Anti-oxidative Regulation Of Edaravone On Sepsis-associated Encephalopathy In Rats

Objective We aimed at studying the mechanism of Sepsis-associated encephalopathy (SAE) in Cecal ligation and puncture (CLP) rat model, and evaluating the therapeutic effect of Edaravone in SAE.Methods Ninty-nine clean level SD male rats were randomly divided into six group:norm group, sham group, no-SAE group, SAE group, ED1group, ED2group. Delta activity percentage of EEG and Neurological scoring were used for the diagnosis of SAE. On24h, brain tissue homogenate is made for monitoring SOD, MDA, COX-2and SDH. Mitochondrion of nerve cells were observed by electronic microscopy and the degree of injury was analyzed by Flameng semi-quantitative evalution of ultrastructure.Results Norm group had nine, sham group had nine, no-SAE group had twelve, SAE group had ten, ED1group had six, and ED2group had six. Delta activity percentage of EEG in CLP rats was growing by the time (P<0.05). The time when ED2group appeared SAE is shorter than SAE group and ED1group (P<0.05). The Neurological scoring in NE group, SAE group, ED1group and ED2group was decreasing after3h, and SAE group decreased fastest. what’s more, ED1group decreased faster than ED2group (P<0.05). The SOD、 MDA、 COX-2、 SDH in NE group and sham group, SAE group and NE group, SAE group and ED1group, SAE group and ED2group, ED2group and ED1group had significant difference with each other (P<0.05). The degree of injury in nerve cell and Mitochondrion among CLP rat is severe. What’s more, SAE is severer. Among ED1group and ED2group, ED2group’s injury was less severer (1.5<3, P<0.05).Conclusion Oxidative stress (especially the alteration in mitochondrial structure and function caused by oxidative stress) might contribute to thedevelopment of SAE; Edaravone exerted a therapeutic effect in SAE by inhibiting oxidative stress and decrease inflammation. What’s more, the more dosage, the more effect.