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. Author manuscript; available in PMC: 2014 Feb 1.
Published in final edited form as: J Neurochem. 2012 Dec 28;124(4):523–535. doi: 10.1111/jnc.12111

Fig. 1.

Fig. 1

Higher oxidative stress increased C3 after tFCI. (a) Relative C3 mRNA levels were measured by QPCR using total RNA extracted from the ischemic brains of mice. mRNA expression was detected using the C3 primer sequences described in the Materials and methods. SOD1 Tg mice had reduced C3 mRNA levels after tFCI compared with WT mice (***p<0.001, n=4, comparison between WT and SOD1 Tg mice at the same time points, ### p<0.001, n=4, compared to WT sham). (b) Relative C3 protein levels were measured by Western blotting after tFCI. β-actin was used as an internal control. In SOD2 KO mice, the amounts of C3 protein were increased up to 3 days and were higher than in the WT mice after tFCI. 4-HNE protein levels were also up-regulated in SOD2 KO mice. The graphs illustrate that C3 proteins, including C3 α-chain and β-chain, were significantly increased in the SOD2 KO mice after tFCI (***p<0.001, n=4, comparison between WT and SOD2 KO mice at the same time points, ### p<0.001, n=4, compared to WT sham).