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. 2023 Nov 8;14:1240352. doi: 10.3389/fphys.2023.1240352

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Copyright © 2023 Packialakshmi, Burmeister, Anderson, Morgan, Cannon, Kiang, Feng, Lee, Stewart and Zhou.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Hemorrhage potentiates TILLIR-induced injury in the renal cortex. (A) Representatives of TILLIR-induced renal tubular degeneration and necrosis. Increased hematoxylin/eosin staining indicates tubular degeneration and necrosis (arrow). (B) Compared with Control, TILLIR increased renal tubular degeneration and necrosis, but hemorrhage had no additive effect. (C) Representatives of TILLIR-induced increase of KIM-1 immunohistochemical staining. (D) TILLIR did not significantly increase KIM-1 protein abundance in the absence of hemorrhage. However, it showed a significant increase in KIM-1 protein abundance in the presence of hemorrhage when compared to the hemorrhage only group. In A and B, n = 6 for the control, n = 8 for the hemorrhage only, n = 9 for the tourniquet only and hemorrhage + tourniquet, respectively. In (C,D), n = 8. *p < 0.05, Two-way ANOVA. Scale bars: 20 µm.