Department of Ophthalmology, Shijiazhuang Third Hospital, Shijiazhuang, Hebei, China.
Department of Endocrinology, Shijiazhuang First Hospital, Shijiazhuang, Hebei, China.
Pak J Pharm Sci. 2020 Sep;33(5(Special)):2431-2437.
This study was aimed to investigate whether fasudil can protect retinal ganglion cells and promote axonal regeneration by inhibiting RhoA/Rock pathway. Long Evans rats were used to establish an optic nerve injury model. Apoptosis was detected by TUNEL, and surviving RGCs was detected by Fluoro-Gold retrograde label and hematoxylin-eosin (HE) staining was used to evaluate pathological changes and western blot was used to measure the expression of protein. After 10 days of optic nerve injury rat model, increased cell apoptosis and decreased FG-positive RGCs in rat eye, but fasudil could reverse these changes. In vitro, fasudil could not only increase the number of RGCs with protuberances, but also increase the length of protuberances. Moreover, fasudil could not only reduce the expression of total-cohoin, Rock, total-cofilin and total-MLC protein induced by optic nerve injury, but also reduce the relative expression of GTP-RhoA, p-cofilin and p-MLC protein. Fasudil protects retinal ganglion cells and promotes axonal regeneration by inhibiting RhoA / Rock pathway.
本研究旨在探讨法舒地尔是否通过抑制 RhoA/Rock 通路来保护视网膜神经节细胞并促进轴突再生。Long Evans 大鼠被用于建立视神经损伤模型。通过 TUNEL 检测细胞凋亡，通过荧光金逆行标记法检测存活的 RGCs，并用苏木精-伊红（HE）染色评估病理变化，并用 Western blot 测量蛋白表达。视神经损伤大鼠模型 10 天后，大鼠眼中细胞凋亡增加，FG 阳性 RGCs 减少，但法舒地尔可逆转这些变化。体外，法舒地尔不仅可以增加有突起的 RGCs 数量，还可以增加突起的长度。此外，法舒地尔不仅可以降低视神经损伤诱导的总肌球蛋白轻链激酶、Rock、总丝切蛋白和总肌球蛋白轻链蛋白的表达，还可以降低 GTP-RhoA、p-丝切蛋白和 p-肌球蛋白轻链蛋白的相对表达。法舒地尔通过抑制 RhoA/Rock 通路来保护视网膜神经节细胞并促进轴突再生。
