IL-6 Deficiency Attenuates Skeletal Muscle Atrophy by Inhibiting Mitochondrial ROS Production through the Upregulation of PGC-1α in Septic Mice

Figure 3

IL-6 KO inhibited mitochondrial ROS production and upregulated PGC-1ɑ expression in septic mice. (a) Mitochondrial ROS production in EDL was measured at the end of experiment; (b) correlation analysis revealed a positive association between IL-6 mRNA expression and mitochondrial ROS production; RT-PCR (c) and western blots (d) were performed to measure the mRNA and protein expressions of PGC-1ɑ in EDL; (e) correlation analysis revealed a negative association between IL-6 mRNA expression and PGC-1ɑ mRNA expression; (f) mitochondria-targeted antioxidant MitoTempol (MitoT) abolished CLP-induced mitochondrial ROS production; (g) MitoTempol treatment increased CSA of myofibers of septic mice; (h) MitoTempol treatment improved muscle force-generating capacity of mice subjected to CLP. CLP: cecal ligation and puncture. , ; (ANOVA followed by unpaired Student -test, ).

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