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. 2018 May 29;8:8346. doi: 10.1038/s41598-018-26421-5

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Establishment of cerebral ischemic reperfusion (I/R) injury model in diabetic rats. SD rats were randomly divided into 4 groups: Control-sham, Control-I/R, DM-sham, DM-I/R. The diabetic rats (n = 12) were induced by intraperitoneal injection of streptozotocin (STZ, 60 mg/kg). The another 12 rats were received the equal volume of citrate buffer. The cerebral I/R injury models in diabetic rats (DM-I/R, n = 6) were established by middle cerebral artery occlusion (MCAO). The diabetic rats were sham operated, as control for cerebral I/R injury (DM-sham, n = 6). The rats with citrate buffer received MCAO (Control-I/R, n = 6) and sham operation (Control-sham, n = 6), respectively. (A) The functional neurological deficit score was assessed and (B) the brain edema was determined at 24 and 72 hours after cerebral I/R injury. (C) A schematic of the peri-infarct area. 1: peri-infract cortex; 2: ischemic core. The secretion levels of (D) TNF-α, (E) IL-1β and (F) IL-6 in the peri-infarct cortical tissues were detected by ELISA assay. *P < 0.01 vs. Control-sham; ^#P < 0.01 vs. Control-I/R.