Reducing Heart Failure in Acute Myocardial Infarctionby Downregulating SOX6 Expression via Nuclear Factor-κB

Our aim was to investigate the mechanisms of SRY-Box Transcription Factor 6 (SOX6) in heart failure (HF) in acute myocardial infarction (AMI).

Sixty healthy people and 60 patients with AMI were divided into the control and AMI groups, and SOX6 expression levels were measured. Hypoxia-induced rat cardiomyocytes (H9c2 cells) were used to construct AMI cell models and split into the blank (control), Hypoxia, Hypoxia + si-NC, Hypoxia + si-SOX6, Hypoxia + pcDNA3.0, Hypoxia + SOX6, Hypoxia + si-SOX6 + HY-18739 and Hypoxia + SOX6 + M4005 groups. The cell viability, reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) levels, apoptosis, SOX6 mRNA expression, collagen I, collagen IV, fibronectin, p-IκBα, p-p65 and SOX6 protein expression levels were compared in the H9c2 cells.

The SOX6 mRNA and protein expression were elevated in the AMI and Hypoxia groups. The cell viability and SOD level decreased, and ROS, MDA level, apoptosis rate, collagen I, collagen IV and fibronectin protein expression level increased in the Hypoxia and Hypoxia + SOX6 groups. The cell viability, SOD level, ROS, MDA level, apoptosis rate, collagen I, collagen IV, fibronectin and SOX6 protein expression level were increased in the Hypoxia + si-SOX6 and Hypoxia + SOX6 + M4005 groups. The p-IκBα and p-p65 protein expression were decreased in the Hypoxia + si-SOX6 group and increased in the Hypoxia + si-SOX6 + HY-18739 group.

Downregulation of SOX6 expression attenuates HF during acute myocardial infarction via the nuclear factor-κB (NF-κB) signal pathway. It could provide a reference basis for early diagnosis and targeted therapy of HF in AMI.