Objective:
To study the protective mechanism of oxymatrine on
oxidative stress induced by high
glucose in H9C2
cells.
Method:
H9C2
cardiomyocytes were cultured in groups and divided into normal group, high
glucose (HG) group, low-
dose oxymatrine (OMT) group (50 mg·L-1), high-
dose OMT group (100 mg·L-1), positive
drug vitamin E (VE) group (1×10-4 mol·L-1) and
mannitol (M) wasotonic
control group.
Cell damage was detected by
lactate dehydrogenase leakage, changes in
cell superoxide dismutase (SOD) activity and
malondialdehyde (MDA) content were detected, intracellular
reactive oxygen species (ROS) content and cellular
mitochondria and functional integrity were detected by
fluorescent probes, and
Western blotting was used to detect the expressions of Bcl
family proteins.
Result:
Compared with the normal group, the content of
malondialdehyde and
reactive oxygen species and the expression level of
pro-apoptotic protein in the high
glucose group were significantly increased (P<0.01), while the activity of
superoxide dismutase and the expression levels of
mitochondrial membrane potential (
MMP) and
anti-apoptotic protein were significantly decreased (P<0.01). Compared with the high
glucose group, oxymatrine significantly reduced the
leakage of
lactate dehydrogenase, significantly inhibited the
production of intracellular ROS (P<0.01), reduced the amount of
malondialdehyde and down-regulated the expression of
pro-apoptotic protein (P<0.05), increased the activity of
superoxide dismutase, regulated
MMP and improved the expression of
anti-apoptotic protein (P<0.01).
Conclusion:
Oxymatrine can regulate
oxidative stress by improving mitochondrial function, so as to inhibit the
apoptosis of H9C2
cardiomyocytes induced by high
glucose.