| Objective To investigate the role of high mobility group protein 2（HMGA2） in lipopolysaccharide（LPS）-induced cardiomyocyte injury and its underlying mechanism. Methods H9c2 cardiomyocytes were divided into four groups: a control group, an LPS group, an Ad-HGMA2 overexpression group, and an Ad-HMGA2+LPS group. H9c2 cardiomyocytes were stimulated by LPS（100 ng/mL） to induce cell injury. A lactate dehydrogenase（LDH） kit was used to detect cell injury, CCK8 was used to detect cell survival rate, and commercial kits were used to detect cell related inflammation and reactive oxygen species indicators such as tumor necrosis factor（TNF）, interleukin-1（IL-1）, interleukin-6（IL-6）, reactive oxygen species（ROS）. Malondialdehyde（MDA） was used to detect the degree of lipid peroxidation; glutathione（GSH） and glutathione peroxidase（GPX） were used to detect the redox status of cells; the content of ferrous ions(Fe2+) in cells was detected by colorimetry; the nuclear translocation rate of p53 was detected by immunofluorescence staining. Results Compared with the LPS group, the activity of LDH in the Ad-HMGA2+LPS group decreased, and the cell survival rate was improved（P<0.05）, Compared with the LPS group, the levels of TNF, IL-1, IL-6, ROS and MDA in the Ad-HMGA2+LPS group were significantly decreased, while the levels of GSH and GPX were significantly increased（P<0.05）. The Fe2+content of myocardial cells in the Ad-HMGA2+LPS group was significantly lower than that in the LPS group, and the p53 nuclear translocation rate was also reduced（P<0.05）. Conclusion HMGA2 can alleviate LPS-induced myocardial injury by inhibiting the p53-ferroptosis pathway. |
