OBJECTIVE: To observe the effects of minocycline on morphology and the expression of synaptophysin in cortical tissues of rats after cerebral ischemia reperfusion injury. METHODS: 36 male SD rats were randomly divided into 3 groups: sham group, model group [ischemia reperfusion (I/R)] and minocycline (Min) group (treated with minocycline for 14 d, 3 mg/kg, 2 times/d ). Middle cerebral artery occlusion (MCAO) was used to established as focal cerebral I/R model. At 14 d after I/R. Neurological functional recovery was evaluated using the staircase test, the cell morphology in cortex was evaluated by HE staining, the neurite growth was observed by immunostaining with anti-microtubule-associated protein-2 (MAP-2) antibody, the expression of synaptophysin in pei-infarct region was tested by Western blot. RESULTS: In the sham group, the rats did not show any neurological deficits. The neurons in the cortex were arranged in neat rows and the morphology were normal, the MAP-2 positive neurons showed longer neuronal processes than the model group. Compared to the model group, minocycline significantly improved forelimb motor function, increased the expression of synaptophysin and the number of MAP-2-positive cells in peri-infarct region (P < 0.05). CONCLUSION: Minocycline could improve the neurite regrowth and the expression of synaptophysin of neuron in ischemic cortex, promote neurological functional recovery of rats after MCAO, which is related to regulate the neuronal plasticity.
OBJECTIVE: To observe the effects of minocycline on morphology and the expression of synaptophysin in cortical tissues of rats after cerebral ischemia reperfusion injury. METHODS: 36 male SD rats were randomly divided into 3 groups: sham group, model group [ischemia reperfusion (I/R)] and minocycline (Min) group (treated with minocycline for 14 d, 3 mg/kg, 2 times/d ). Middle cerebral artery occlusion (MCAO) was used to established as focal cerebral I/R model. At 14 d after I/R. Neurological functional recovery was evaluated using the staircase test, the cell morphology in cortex was evaluated by HE staining, the neurite growth was observed by immunostaining with anti-microtubule-associated protein-2 (MAP-2) antibody, the expression of synaptophysin in pei-infarct region was tested by Western blot. RESULTS: In the sham group, the rats did not show any neurological deficits. The neurons in the cortex were arranged in neat rows and the morphology were normal, the MAP-2 positive neurons showed longer neuronal processes than the model group. Compared to the model group, minocycline significantly improved forelimb motor function, increased the expression of synaptophysin and the number of MAP-2-positive cells in peri-infarct region (P < 0.05). CONCLUSION:Minocycline could improve the neurite regrowth and the expression of synaptophysin of neuron in ischemic cortex, promote neurological functional recovery of rats after MCAO, which is related to regulate the neuronal plasticity.