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. 2017 Jun 30;26(7):1276–1285. doi: 10.1177/0963689717716510

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© The Author(s) 2017

This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (http://www.creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Figure 2. — The expression of Tnr, Trim32, and cytochrome c oxidase polypeptide 5A (COX5A) at different time points after traumatic brain injury (TBI) in rats. (a) Reverse transcription polymerase chain reaction (RT-PCR) results in injured cortex and sham-operated rats. β-Actin was used as control. Marker was in the left side and then from left to right is sham, 1 h, 6 h, 24 h, and 7 d postoperation, respectively. The bands (7 d postoperation) are obviously brighter than others. (b to d) The messenger RNA (mRNA) expression of Trim32, Tnr, and COX5A in the cortex. β-Actin was used as control. (e) This is to exhibit the protein level of Trim32. β-Actin was used as control. Lane 1 in the left side displays the protein band in the sham-operated group, and lanes 2 to 5 show the protein band at 1 h, 6 h, 24 h, and 7 d postoperation, respectively. The relative translation of Trim32 was higher in 7 d postoperation. *P < 0.05 compared with the sham group.