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. 2020 Sep;8(18):1136. doi: 10.21037/atm-20-5115

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2020 Annals of Translational Medicine. All rights reserved.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0.

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Ulinastatin exerts protective effects against cerebral I/R injury via activation of the Nrf-2/HO-1 signaling pathway. SD rats were divided into the sham, MCAO, ulinastatin, ML-385, and ulinastatin + ML-385 groups. Cerebral I/R injury was induced by MCAO and SAH. Before surgery, 50 pmol of ML-385 was injected, and after surgery, ulinastatin was administered at a dosage of 300,000 U/kg 15 min. Brain tissues and serum were collected from the rats. (A) HE and TUNEL staining of the brain tissues were observed, scale bar: 50 μm. (B) The concentrations of IL-6, IL-1β, and IL-18 in the serum were tested with ELISA. The serum levels of SOD (C), MDA and GSH (D), and ROS (E) were analyzed. The bars show means ± SD of at least three independent experiments. **, P<0.01 compared with the sham group; ^##, P<0.01 compared with the MCAO group.