Research Paper Volume 16, Issue 6 pp 5207—5223
Allicin treats myocardial infarction in I/R through the promotion of the SHP2 axis to inhibit p-PERK-mediated oxidative stress
Figure 4. Transcriptomic sequencing has revealed the gene expression profile of in situ macrophages during the treatment of myocardial ischemia-reperfusion in mice with allicin. The gene SHP2 is significantly upregulated with the treatment of allicin, affecting the protection exerted by allicin in ischemia/reperfusion (I/R) conditions. (A) Intersection of datasets GSE171821 and GSE108940 revealed SHP2 as one of the critical genes within the intersection. (B) Volcano plots in heatmaps demonstrated the most significant difference in the expression of SHP2 mRNA in myocardial ischemia/reperfusion (MI/R) + allicin treatment. (C) GO analysis showed that kinase-mediated signaling pathways and oxidative stress-mediated signaling pathways had the most noticeable changes in allicin-treated mouse hearts under ischemia-reperfusion. (D) KEGG analysis indicated that virus-related macrophage signaling pathways were the most significantly altered in allicin-treated mice experiencing heart ischemia-reperfusion.