| Objective:The ischemia/reperfusion injury of Coronary artery disease is alwaysaccompanied by myocardial hypoxia/reoxygenation process，which eventuallylead to apoptosis.How to alleviate the myocardial injury produced by thisprocess is a research hotspot in recent years. This experiment based on activityof myocardial cells and detect interleukin-6(IL-6) and tumor necrosisfactor alpha (TNF-α)，to analysis the pathological changes of myocardialischemia/reperfusion injury and the related mechanism.Futher, to discuss thedefend effect of oxocamphor on myocardial cells after ischemia/reperfusioninjury.Methods:Rat myocardial cell(H9c2) oxygen deprivation and reperfusion modelwere randomly divided into four groups: normal group, hypoxia group, hypoxia+oxocamphor group A, hypoxia+oxocamphor group B. Normal control group:no special treatment; Hypoxia group: oxygen deprivation was perfomed byputting cells in hypoxic incubater（5%CO2；95%N2，37.0℃）for4h. oxygendeprivation was terminated by removing cells from anoxia incubater,replenishing with normal media, and replacing them back into normoxicincubator（5%CO2；95%空气，37.0℃）for4h. Hypoxia+oxocamphor group:20ul/50ml (group A),30ul/50ml (group B) oxocamphor were added intothe cardiac cells after hypoxia/reperfusion. Each group myocardial cell viability was detected by2,3bis(2methoxy4nitro5sulfophenyl)5〔(phenylamino)Carbonyl〕2H tetrazolium hydroxide assay (XTT). Celldamage was evaluated by IL—6and TNF-αimmunocytochemistry staining（MaxVision）.Statistics:measurement data show as x±S, use paired t-test to compared pre andpost treatment, groups data use t-test.A value of P <0.05was consideredsignificant.Results:1.H9c2cells were cultured in oxygen deprivation condition for6h. XTTassay showed that the absorbency value (A value) in hypoxia group was lowerthan control group (P <0.05);absorbency value (A value) in hypoxia group waslower than hypoxia+oxocamphor group(P <0.05); absorbency value (A value)in hypoxia+oxocamphor group was lower than control group (P <0.05);Moreover, The cell viability in hypoxia+oxocamphor group B was higher thanthat in hypoxia+oxocamphor group A.2. IL-6protein expression was the lowest in the control group and thehighest in hypoxia group.IL-6protein expression was significantly lower inhypoxia+oxocamphor group than hypoxia group, which was lower in hypoxia+oxocamphor group B compared to hypoxia+oxocamphor group A.3. TNF-αprotein expression was the lowest in the control group and thehighest in hypoxia group. Also, TNF-α protein expression was significantlylower in hypoxia+oxocamphor group than in hypoxia group, which was lowerin hypoxia+oxocamphor group B compared to hypoxia+oxocamphor groupA. Conclusions:Oxocamphor is benefit to hypoxia induced myocardial cell injury. Andthat is mediated by attenuation of oxidative cell damage and inhibition ofapoptosis. |
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