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. 2022 Mar 14;13:856699. doi: 10.3389/fphys.2022.856699

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Copyright © 2022 Qin, Liu, Gao, Hu, Chen, Xu and Zhang.

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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Protein kinase C isoform PKCε is identified as the direct target of GDL by functional analysis. (A) Representative Western blot images of ERK expression and phosphorylation in H/R-injured NRCM cells following the treatment of PKC inhibitors (Chelerythrine, Gö6976, Rottlerin or PKCεV1-2). (B) Quantification analysis of ERK phosphorylation in H/R-injured NRCM cells following PKCεV1-2 treatment. (C,D) Immunofluorescence staining of PKCε nuclear translocation in the heart of mice treated with or without GDL. (E) The effect of PKCεV1-2 on GDL-induced cardioprotection against H/R injury. *P < 0.05 and **P < 0.01 between indicated groups. Data shown are representive of five independent experiments.