Cardioprotective Effect of circ_SMG6 Knockdown against Myocardial Ischemia/Reperfusion Injury Correlates with miR-138-5p-Mediated EGR1/TLR4/TRIF Inactivation

Figure 6

EGR1 silencing diminishes neutrophil recruitment and alleviates I/R injury by inactivating the TLR4/TRIF signaling pathway. (a) Transcriptional binding sites of EGR1 in the TLR4 promoter predicted by the hTFtarget website. (b) Expression of TLR4 and TRIF determined by qRT-PCR in myocardial tissues of sham-operated mice, I/R mice, and sh-EGR1-treated I/R mice. I/R mice were treated with sh-EGR1, resatorvid, and sh-EGR1 + oe-TLR4. (c) Representative microscopic views of neutrophil (green) migration process on the myocardial vascular wall in I/R mice under a two-photon microscope (the vessel was in red). (d) The rolling speed of neutrophils in the blood vessel of I/R mice. (e) The density of neutrophils in I/R mice. (f) The exudation ratio of neutrophils in I/R mice. (g) Detection of LVSP, LVDP, +dp/dtmax, and -dp/dtmax related to cardiac function in I/R mice. (h) LVFS% and LVEF% detected by electrocardiogram in I/R mice. (i) Activity of LDH and CK in the arterial blood of I/R mice. (j) TTC staining of myocardial tissues of I/R mice. (k) Apoptosis of cardiomyocytes in myocardial tissues of I/R mice assessed by TUNEL assay. vs. the sham-operated mice or I/R mice treated with sh-NC. # vs. the I/R mice treated with sh-NC or sh-EGR1. for mice following each treatment.

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