Research Paper Volume 13, Issue 10 pp 14219—14233

LncRNA AK020546 protects against cardiac ischemia–reperfusion injury by sponging miR-350-3p

MiR-350-3p reversed the effect of lncRNA AK020546 on cardiac I/R injury in vitro. (A, B) qPCR was used to assess the level of miR-350-3p in H9c2 cardiomyocytes under different treatments (n = 5). (B, C) Flow cytometry and Annexin V/propidium iodide (PI) staining were performed to detect the apoptosis of H9c2 cardiomyocyte (n = 5). (D) TUNEL staining was performed to detect the apoptosis of specific H9c2 cardiomyocytes (n = 5). (E–G) The levels of oxidative markers such as LDH, MDA, and ROS were assessed with commercial kits (n = 5). (H, I) JC-1 staining was performed to evaluate the mitochondrial membrane potential (n = 5). (J) MitoSOX staining was used to evaluate the mitochondrial ROS. *p #p 2O2 group, &p

Figure 6. MiR-350-3p reversed the effect of lncRNA AK020546 on cardiac I/R injury in vitro. (A, B) qPCR was used to assess the level of miR-350-3p in H9c2 cardiomyocytes under different treatments (n = 5). (B, C) Flow cytometry and Annexin V/propidium iodide (PI) staining were performed to detect the apoptosis of H9c2 cardiomyocyte (n = 5). (D) TUNEL staining was performed to detect the apoptosis of specific H9c2 cardiomyocytes (n = 5). (EG) The levels of oxidative markers such as LDH, MDA, and ROS were assessed with commercial kits (n = 5). (H, I) JC-1 staining was performed to evaluate the mitochondrial membrane potential (n = 5). (J) MitoSOX staining was used to evaluate the mitochondrial ROS. *p < 0.05 vs control, #p < 0.05 vs H2O2 group, &p < 0.05 vs AK020546 + miR-nc group.