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. 2021 Jun 25;8:660269. doi: 10.3389/fmolb.2021.660269

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Copyright © 2021 Xu, Ma and Yang.

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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CircTLK1 induces sepsis-related AKI by the miR-106a-5p/HMGB1 axis. (A–C) The CLP-induced sepsis-related AKI rat model was established in Wistar rats (N = 6), followed by the indicated treatment. The cecum was exposed without perforation in the sham groups. (A) qPCR analysis of HMGB1 expression. (B) H&E staining of kidney tissues, bar = 50 μm. (C) TUNEL assays of apoptosis analysis in the rats, bar = 50 μm. (D–G) For the induction of the cell injury model, the HK-2 cells were treated with LPS (1 mg/L) for 24 h after the cell concentration reached 80%, followed by the indicated treatment. (D) qPCR analysis of HMGB1 expression. (E) Western blot analysis of TNF-α, IL-1β, and IL-6. (F) Western blot analysis of Bax, Bcl-2, and cleaved caspase-3. (G) Flow cytometry analysis of apoptosis, mean ± SD, **P < 0.01, ***P < 0.001.