| Objective To study the influence and mechanism of minocycline on morphology and ultrastructure of the ischemia-reperfiision brain tissue of gerbils.Methods A cerebral ischemia-reperfusion model in gerbils was established by clamping both common carotids. Fifty gerbils were randomly divided into: normal control group,sham operation group, ischemia-reperfusion(IR) group, minocyline intervention group Minocycline treated subjects were injected with a dose (45 mg/kg i.p, BID) of the minocycline, starting 1 day before the ischemic episode till sacrificed.The gerbils were sacrificed in batch and the brain tissues were quickly obtained to make the samples at the 6th hour, 1st day, 3rd and 7th day after ischemia-reperfusion. Ultrastructural alteration in pyramidal neuron in the hippocampal CA1 and the cortex of frontal lobe were examined in gerbils after 10 minutes transient forebrain ischemia by electron microscope.The expressions of phosphorylation P38MAPK were also taken in gerbils models postocclusion by using immunohistochemistry technique.All results were analyzed with Spssl2.0.Results 1. Debris, vacuole and irregular chromatin condensation were found in all neurons postocclusion. Swollen of mitochondria,endoplasmic reticulum and Golgi complex were observed in gerbils models 6h postocclusion.Pyknotic and karyolysis were also emerged in 3 and 7 days postocclusion.The damage to the brain became more and more severe as gerbils survived longer postocclusion.There was a significant difference between gerbils 6h,1day postocclusion and gerbils models of 3,7 days postocclusion ( p < 0.05 ) ,but no significant difference was found between gerbils 6h and 1day postocclusion(P > 0.05). Significant difference was also observed between IR and minocyline treated groups ( p < 0.01).2.Results revealed that phosphorylation P38MAPK was expressed in both of the neurons and gliacytes in gerbils. The expression level of phosphorylation P38MAPK was low in normal control group and sham operation group, which increased as the gerbils suvived longer, especially in gerbils 3 and 7 days postocclusion with a significant difference ( p < 0.01) .Treatment with minocycline reduced expression of phosphorylation P38MAPK with a significant difference ( p < 0.05).Conclusions 1. Swollen, disrupt and necrosis of organelles were found in pyramidal neurons of the hippocampal CA1 and the cortex of frontal lobe in gerbils following transient forebrain ischemia.2. Minocycline reduced the ultrastructural damage to brain tissue after ischemic insults, indicating its neuroprotective effect.3. Minocycline may exert neuroprotection by decreasing expression of phosphorylation P38MAPK. |
