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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.2.

Fig.2

The antioxidant PBN suppressed C3 levels after tFCI. The vehicle and PBN were injected 1 h prior to onset of tFCI and every 24 h after tFCI. (a) tFCI increased C3 mRNA levels in the vehicle-treated group. In the PBN- pre treated group, the relative C3 mRNA level was reduced compared with the vehicle-treated group (***p<0.001, n=6, compared to PBN 0 mg/kg-treated mice at the same time points; -fold to sham 24 h) (b) Post treatment of PBN also significantly decreased C3 mRNA levels after tFCI compared to vehicle-treatment (***p<0.001, n=4, compared to vehicle-treated mice at the same time points; -fold to vehicle sham. Veh indicates vehicle. (c) Western blot analysis showed that the increase in C3 was markedly suppressed by PBN after tFCI. 4-HNE levels were down-regulated by PBN (***p<0.001, n=6, comparison between vehicle- and PBN-treated mice at the same time points; -fold to vehicle-sham). (d) C3 blood levels increased after tFCI and were reduced by antioxidant. Blood from mice were collected after tFCI followed by 24 h and 3 days reperfusion, plasma isolated, and C3 levels were measured by ELISA ( ***p< 0.001, n = 4, compared to PBN 0 mg/kg-treated mice at the same time point; -fold to sham 24 h).