AIM To investigate the effect of dexmedetomidine on the expression of contraction protein in hypoxia-treated cardiomyocytes and its molecular mechanism.
METHODS H9c2 cells were cultured with hypoxia to establish hypoxic injury. The cells were divided into blank control group, hypoxia culture group, hypoxia + dexmedetomidine low dose (0.01 μmol/L) group, hypoxia + dexmedetomidine medium dose (1 μmol/L) group, and hypoxia + dexmedetomidine high dose (100 μmol/L) group. Except for those in the blank control group, the cells in other groups were cultured in 50 ml/L oxygen environment to establish a cell hypoxia injury model. 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-M levels in culture medium and Western blot was used to detect the expressions of titin, β-MHC, PI3K, Akt, p-PI3K and p-Akt protein.
RESULTS Compared with those in the normal control group, the cell survival rate was decreased and apoptosis and the level of myocardial zymogram protein were increased in hypoxic culture group (P<0.01). Compared with those in the hypoxic culture group, the cell survival rate was increased (P<0.05, P<0.01) and apoptosis and the myocardial zymogram protein level in the hypoxic + dexmedetomidine groups were decreased (P<0.05, P<0.01). Western blot showed that compared with those in the hypoxic culture group, the expressions of p-PI3K and p-Akt were increased, while the expressions of titin and β-MHC were decreased in a dose-dependent manner in dexmedetomidine-treated H9c2 cells under hypoxic condition (P<0.05).
CONCLUSION Dexmedetomidine inhibits contractile protein expression in hypoxia-injured cardiomyocytes, and whether the mechanism is related to activation of PI3K/Akt signaling pathway needs further study.
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