AIM  To study the effect of dexmedetomidine (DEX) on the expression of contractile protein and its molecular mechanism after hypoxia injury.

  METHODS  H9C2 cells were cultured under 50 ml/L oxygen concentration to establish hypoxic injury. The experiment was divided into control group, hypoxia group, hypoxia + DEX (0.01 μmol/ml, 1 μmol/ml, 100 μmol/ml) group. In addition to the control group in normal cell environment, the remaining four groups were cultured in hypoxia environment, and three groups were added with corresponding concentrations of DEX as required. MTT method was used to measure cell survival rate, flow cytometry was used to detect apoptosis level, ELISA was used to detect cTnI, LDH and CK-MB levels in culture medium, the expression of titin, β-MHC, PI3K, Akt, p-PI3K, p-Akt protein in H9C2 cells were detected by Western blot.

  RESULTS  Myocardial cell injury was induced successfully, compared with the normal control group, the cell survival rate was decreased, apoptosis was increased, and the level of zymogram protein in the center of the culture medium increased; compared with the hypoxic culture group, the cell survival rate, apoptosis and myocardial zymogram protein level of the hypoxic + dexmedetomidine groups were increased; Western blot showed that the expression of p-PI3K and p-Akt were increased, while the expression of titin and β-MHC were decreased, and all this is in a dose-dependent manner.

  CONCLUSION  Dexmedetomidine regulates the expression of contractile protein in hypoxic myocardial cells, which may be related to the PI3K/Akt signaling pathway. Whether it is associated with activation of PI3K/Akt signaling, further research is needed.