To investigate the functional role of fasudil in optic nerve crush (ONC), and further explore its possible molecular mechanism. After ONC injury, the rats were injected intraperitoneally either with fasudil or normal saline once a day until euthanized. RGCs survival was assessed by retrograde labeling with FluoroGold. Retinal glial cells activation and population changes (GFAP, iba-1) were measured by immunofluorescence. The expressions of cleaved caspase 3 and 9, p-ERK1/2 and p-AKT were detected by western blot. The levels of the pro-inflammatory cytokines were determined using real-time polymerase chain reaction. Fasudil treatment inhibited RGCs apoptosis and reduced RGCs loss demonstrated by the decreased apoptosis-associated proteins expression and the increased fluorogold labeling of RGCs after ONC, respectively. In addition, the ONC + fasudil group compared had a significantly lower expression of GFAP and iba1 compared with the ONC group. The levels of pro-inflammatory cytokines were significantly reduced in the ONC + fasudil group than in the ONC group. Furthermore, the phosphorylation levels of ERK1/2 and AKT (p-ERK1/2 and p-AKT) were obviously elevated by the fasudil treatment. Our study demonstrated that fasudil attenuated glial cell-mediated neuroinflammation by up-regulating the ERK1/2 and AKT signaling pathways in rats ONC models. We conclude that fasudil may be a novel treatment for traumatic optic neuropathy.

探讨法舒地尔在视神经挤压术（ONC）中的功能作用，并进一步探讨其可能的分子机制。ONC损伤后，每天给大鼠腹膜内注射法舒地尔或生理盐水直至安乐死。通过用FluoroGold逆行标记评估RGC的存活。通过免疫荧光测量视网膜胶质细胞的活化和种群变化（GFAP，iba-1）。通过western blot检测半胱天冬酶3和9的表达，p-ERK1 / 2和p-AKT的表达。使用实时聚合酶链反应确定促炎细胞因子的水平。法舒地尔治疗分别抑制ONC后RGCs的凋亡相关蛋白表达降低和氟金标记的增加，从而抑制了RGCs的凋亡并降低了RGCs的损失。此外，与ONC组相比，ONC + fasudil组的GFAP和iba1表达明显降低。与ONC组相比，ONC +法舒地尔组的促炎细胞因子水平显着降低。此外，通过法舒地尔处理，ERK1 / 2和AKT（p-ERK1 / 2和p-AKT）的磷酸化水平明显升高。我们的研究表明，法舒地尔可通过上调大鼠ONC模型中的ERK1 / 2和AKT信号通路来减轻神经胶质细胞介导的神经炎症。我们得出的结论是，法舒地尔可能是创伤性视神经病变的一种新型治疗方法。法舒地尔治疗后ERK1 / 2和AKT（p-ERK1 / 2和p-AKT）的磷酸化水平明显升高。我们的研究表明，法舒地尔可通过上调大鼠ONC模型中的ERK1 / 2和AKT信号通路来减轻神经胶质细胞介导的神经炎症。我们得出的结论是，法舒地尔可能是创伤性视神经病变的一种新型治疗方法。法舒地尔治疗后ERK1 / 2和AKT（p-ERK1 / 2和p-AKT）的磷酸化水平明显升高。我们的研究表明，法舒地尔可通过上调大鼠ONC模型中的ERK1 / 2和AKT信号通路来减轻神经胶质细胞介导的神经炎症。我们得出的结论是，法舒地尔可能是创伤性视神经病变的一种新型治疗方法。