[Myocardial cells and mitochondrial autophagy in sepsis mice induced by lipopolysaccharide].

Objective: To investigate the alterations in the level of myocardial cells and mitochondrial autophagy during myocardial injury in lipopolysaccharide (LPS)-induced septic animal models.

Methods: Male C57BL/J mice were randomly divided into negative control group (NC), LPS treatment groups (6, 12, 24, 36 hours). The LPS treatment groups were subjected to LPS (10 mg/kg) injection intraperitoneally, and the NC group was injected intraperitoneally with the same amount of saline. The mice were sacrificed at the above time points to collect blood and heart tissues. Cytoplasmic protein, mitochondria and mitochondrial proteins were extracted from the myocardial tissue, and other myocardial tissue was frozen for next analysis. Cardiac troponin I (cTnI) levels in sera were evaluated by ELISA; mitochondrial membrane potential (MMP) was tested by JC-1 staining and fluorescence cytometry at different time points after LPS intraperitoneal injection. Furthermore, the levels of autophagy-related proteins such as microtubule-associated protein 1 light chain 3 (LC3), PTEN-induced kinase 1 (pink1), E3-ubiquitin ligase parkin were measured by Western blotting and fluorescent immunohistochemistry.

Results: Compared with the control group, the serum levels of cTnI induced by LPS were significantly higher as 6 hours, while the MMP was significantly lower in the LPS treatment groups, and the lowest was in the 12-hour group. The expression of autophagy-related protein LC3-II/LC3-I significantly increased in the LPS 12-hour treatment group, pink1/parkin was significantly elevated in the LPS 6-hour treatment group, and they then gradually decreased.

Conclusion: The autophagy stress is activated in myocardium during myocardial injury induced by LPS treatment and it probably happens earlier at myocardial mitochondria.