Protective Effect Of Oxacamphor On Oxidative Stress Induced Myocardial Injury

Objective: To analyze the pathological changes and the relevant mecha-nism involved in myocardial ischemia and hypoxia, myocardial ischemiareperfusion, oxidative stress induced myocardial cells damage,8-OHDG(8-oxodeoxyguanosine), the oxidative damage marker and caspase-3, cellapoptosis marker were evaluated. Futher, to detect the effect of oxocamphor onmyocardial cells after oxidative stress injury.Methods: Rat myocardial cell(H9c2) oxygen deprivation and reperfusionmodel were randomly divided into four groups: normal group, hypoxia group,hypoxia+oxocamphor group A, hypoxia+oxocamphor group B. Normalcontrol group: no special treatment; Hypoxia group: oxygen deprivation wasperfomed by putting cells in hypoxic incubater for4h. oxygen deprivation wasterminated by removing cells from anoxia incubater, replenishing with normalmedia, and replacing them back into normoxic incubator for4h. Hypoxia+oxocamphor group:10ul/50ml (group A),20ul/50ml (group B)oxocamphor were added into the cardiac cells after hypoxia/reperfusion. Eachgroup myocardial cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl)2,5-diphenyltetrazolium bromide](MTT) assay. Cell damage was evaluated by8-OHDG and caspase-3immunocytochemistry staining.Statistics:Data is reported as means±SD. Comparisons were made betweendifferent treatment groups and determined by ANOVA, followed by T-test. Avalue of P <0.05was considered significant. Results:1.H9c2cells were cultured in oxygen deprivation condition for4h. MTTassay showed that the absorbency value (A value) in hypoxia group was lowerthan control group (P <0.05).2.In hypoxia+oxocamphor group, cells were cultured for24h thenfollowed by MTT assay. The results showed that in hypoxia group, theabsorbency value (A value) was significantly lower than hypoxia+oxocamphor group, and in hypoxia+oxocamphor group, the absorbency value(A value) was lower than control group (P <0.05). The cell viability in hypoxia+oxocamphor group was significantly higher than that in hypoxia group.Moreover, The cell viability in hypoxia+oxocamphor group B was higher thanthat in hypoxia+oxocamphor group A.3.8-OhdG expression was the lowest in the control group and the highestin hypoxia group. Interestingly,8-OhdG expression was significantly lower inhypoxia+oxocamphor group than hypoxia group, which was lower in hypoxia+oxocamphor group B compared to hypoxia+oxocamphor group A.4. Caspase-3expression was the lowest in the control group and thehighest in hypoxia group. Also, caspase-3expression was significantly lower inhypoxia+oxocamphor group than in hypoxia group, which was lower inhypoxia+oxocamphor group B compared to hypoxia+oxocamphor group A.Conclusions: Oxocamphor is benefit to hypoxia induced myocardial cellinjury. And that is mediated by attenuation of oxidative cell damage andinhibition of apoptosis.