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. 2018 Feb 6;8:2459. doi: 10.1038/s41598-018-20911-2

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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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The effect of thalidomide on infarct volume of the MCAO/R model. (a) Experimental design. Animals underwent 1.5 h of middle cerebral artery occlusion and 24 h reperfusion time (MCAO/R). Thalidomide (20 mg/kg) or DMSO (0.66 ml/kg, vehicle) administration is shown in asterisks. Sample preparation for histological, neurological, and biochemical studies were performed at the end of reperfusion. (b) Representative photographs of TTC-stained brain slices showing the infarct area 24 h after MCAO/R. (c) Quantitative analysis of the infarct area in each slice and the total infarct volume from MCAO/R rats treated with thalidomide or vehicle. The infarct areas caused by MCAO/R were significantly decreased by the administration of thalidomide. Quantification of the infarct volume is represented by mean ± SD (n = 6 for vehicle, n = 5 for thalidomide).