OBJECTIVE: To observe the effect of curcumin pretreatment on myocardial oxidative stress and apoptosis in rats with heat stroke in a dry heat environment and to explore its possible mechanism.
Methods: 50 SD male rats were randomly divided into 5 groups (n=10): normal temperature control group (NC), dry heat control group (DHC), curcumin 50mg/kg pretreatment group (L-cur), curcumin 100 mg/kg (M-cur), curcumin 200 mg/kg (H-cur). The NC and DHC groups were given normal saline by gavage, and the curcumin pretreatment group was given different concentrations of curcumin by gavage, once a day for 7 consecutive days. On the 8th day, except for the NC group, the other 4 groups of rats were transferred to the northwest special environment artificial experimental chamber for the experiment. Heat stroke state, samples were collected after anesthesia, the changes of serum creatine kinase (CK) and lactate dehydrogenase (LDH) were detected by automatic biochemical detector, and myocardial cell apoptosis was detected and calculated by TUNEL method. The levels of myocardial superoxide dismutase (SOD) and malondialdehyde (MAD) were detected, and correlation analysis was performed.
Results: Serum myocardial enzymes CK, LDH, myocardial cell apoptosis index and MDA in dry heat control group were significantly higher than those in normal temperature control group (P<0.01). MDA decreased with the increase of drug concentration, and there were significant differences among curcumin pretreatment groups (P< 0.01); the change trend of SOD was opposite to that of MDA. There was a positive correlation between CK and LDH (correlation coefficients were r=0.30, r=0.30 P<0.05); there was a positive correlation between cardiomyocyte apoptosis and MDA (correlation coefficient was r=0.916, P<0.01); There was a negative correlation between cardiomyocyte apoptosis and SOD (coefficient r=-0.86 P<0.01).
Conclusion: Curcumin pretreatment has a protective effect on myocardial injury in rats with heat stroke in dry heat environment, and curcumin may play a protective effect on myocardial injury by anti-oxidative stress and reducing cell apoptosis.