• Ning Li, Yang Wang, and Qi-yi Zen.
• Department of Neonate, Nanfang Hospital, Southern Medical University, Guangzhou, China. ningli@fimmu.com
• Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2010 Apr 1; 26 (4): 379-81.

AimTo study the pathogenesis of cerebral mitochondrial dysfunction in septi rats.MethodsForty clean level SD male rats were randomly divided into 4 groups: control group, 3-sepsis group, 6 h sepsis group and 24 h sepsis group. The sepsis model was established by intraperitoneal injection of lipopolysaccharide (LPS). The membrane potential of cerebral mitochondrion was detected by flow cytometry. Mitochondrion of four kinds of nerve cells were observed by electronic microscopy and the degree of injury was analyzed by Flameng semiquantitative evaluation of ultrastructure.ResultsCerebral mitochondrial membrane potential in 3-sepsis group decreased significantly compared with that in control group [(0.05 +/- 0.05) vs (1.20 +/- 0.6)], but the brain mitochondrial membrane potential in 6-hour and 24 h LPS group were not significant difference as compared with control group [(1.4 +/- 0.7) vs (1.2 +/- 0.6), (1.6 +/- 0.7) vs (1.2 +/- 0.6)]. Mitochondrial ultrastructure injury evaluation score of neuronal and astroglial in 6 h LPS group rats were increased significantly as compared with control group, but the score of microglial and oligodendroglial in all the 4 groups didn not have significant difference.ConclusionThe injury of rats brain mitochondria was reversible in early sepsis and mitochondrial dysfunction occurred more earlier than the ultrastructure change. Compared with neuronal and astroglial, mitochondrial of microglial and oligodendroglial were more sensitive to septic injury.

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