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. 2021 Mar 8;12:627123. doi: 10.3389/fphar.2021.627123

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Copyright © 2021 Yang, Chen, Yan, Xu, Wu, Pi, Liu, Chai, Li and Dou.

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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TLR4 activation contributes to SAA protection from lipotoxicity-induced injury in cardiomyocytes. Cardiomyocyte cells were treated with PA at 0.4 mM for 4 h. TLR4 was activated with 100 ng/ml LPS for 2 h before PA treatment. 10 μM SAA was added 1 h before PA treatment. (A) Cell viability was tested using MTT. (B) LDH release measurement. (C) Nuclear staining with Hoechst. Cell death was detected by assessing nuclear morphology by fluorescence microscopy at a ×200 magnification (D) ROS levels were measured by DCFH-DA. (E) Mitochondrial membrane potential (MMP) was examined by fluorescence microscopy. (F) Cleaved Caspase-3, TLR4, MyD88, p-JNK, and p-ERK1/2 levels were determined by western blot. Values are presented as mean ± SD for ≥3 independent tests. Bars with different characters are significantly different, p < 0.05.