目的:探讨米诺环素对急性视神经炎的影响,并与甲基强的松龙比较。方法:雌性Wistar大鼠22只随机分为正常组、EAE组、米诺环素组、甲基强的松龙组(MP组)。观察视神经病理改变,免疫组织化学法检测视网膜神经节细胞(retinal ganglion cells,RGCs)中Caspase-3蛋白表达。结果:EAE组视神经光镜下表现为神经纤维空泡样变性,轴突不规则肿胀,大量炎性细胞浸润。EAE组、米诺环素组、MP组与正常组视神经轴突占横切面积比例相比,差异均有显著统计学意义(P<0.01),米诺环素组、MP组与EAE组间的差异均有统计学意义(P<0.05)。正常大鼠视网膜几乎未见Caspase-3蛋白表达,EAE组、MP组与米诺环素组间的差异均有统计学意义(P<0.05),MP组与EAE组间的差异有统计学意义(P<0.05)。结论:甲基强的松龙可减轻脱髓鞘性视神经炎轴突损伤,但不能减少RGCs中Caspase-3的表达。米诺环素可下调Caspase-3在视网膜中表达,提示米诺环素可通过抑制RGCs中Caspase-3活性,介导对脱髓鞘性视神经炎RGCs的保护作用。

AIM:To investigate the effects of minocycline on optic nerve axons and Caspase-3 expression of experimental optic neuritis in Wistar rats.METHODS:Twenty-two female experimental Wistar rats were assigned to four groups randomly:normal group and experimental autoimmue encephalomyelitis group(EAE group),minocycline group,methlprednisolone group(MP group).The pathological changes of optic nerve were observed and the expression of Caspase-3 in retinal ganglion cells(RGCs) was detected by immunohistochemistry.RESULTS:In EAE group,the optic nerve fibers showed bulb-like degeneration,the axis irregular swelling,a quantity of inflammatory cell infiltrating under light microscope.The axons showed bulb-like degeneration,myelin sheaths were loose,microtubule and microfilament disappeared under electron microscopy.The area percentage of axons:there was very significant difference(P<0.01),when EAE group,minocycline group and MP group compared with normal group.There was significant difference(P<0.05),when minocycline group and MP group compared with EAE group.In normal rats,there was little expression of Caspase-3 in retina.There was significant difference(P<0.05),when EAE group and MP group compared with minocycline group.There was significant difference(P<0.05),when MP group compared with EAE group CONCLUSION:Methlprednisolone can reduce demyelinating optic nerve axons injury,but can not reduce the expression of Caspase-3 in RGCs.Minocycline can down-regulate the expression of Caspase-3 in retina,which show that minocycline has a marked protection of RGCs in demyelinating optic neuritis by inhibiting the expression of Caspase-3.

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