【摘要】：目的觀察白皮杉醇對(duì)青光眼大鼠視網(wǎng)膜神經(jīng)節(jié)細(xì)胞(retinal ganglion cells,RGCs)的保護(hù)作用并探討其可能的機(jī)制。方法將40只大鼠隨機(jī)分為對(duì)照組、模型組、白皮杉醇低劑量組和白皮杉醇高劑量組。采用光凝法建立青光眼大鼠模型,白皮杉醇低、高劑量組分別給予100 mg·kg~(-1)和200 mg·kg~(-1)白皮杉醇灌胃。測(cè)量各組大鼠眼壓;熒光金逆行標(biāo)記各組大鼠RGCs并計(jì)數(shù);HE染色觀察各組大鼠視網(wǎng)膜組織病理形態(tài);免疫印跡法檢測(cè)各組大鼠視網(wǎng)膜組織中磷酸化原癌基因蛋白Jun(proto oncogene protein Jun,c-Jun)氨基末端激酶(phosphorylation c-Jun N-terminal kinase,p-JNK)、磷酸化c-Jun(phosphorylation c-jun,p-c-Jun)、磷酸化細(xì)胞外調(diào)節(jié)蛋白激酶(phosphorylation extracellular regulated protein kinases,p-ERK)、磷酸化絲裂原活化蛋白激酶p38(phosphorylation mitogen activated protein kinases p38,p-p38 MAPK)和腫瘤壞死因子-α(tumor necrosis factor-alpha,TNF-α)蛋白表達(dá)。結(jié)果模型組眼壓、p-JNK、p-c-Jun、p-ERK、p-p38 MAPK和TNF-α蛋白表達(dá)均顯著高于對(duì)照組(均為P0.05),RGCs低于對(duì)照組(P0.05),視網(wǎng)膜組織結(jié)構(gòu)可見空泡和水腫樣改變。與模型組相比,白皮杉醇低劑量組和白皮杉醇高劑量組大鼠RGCs顯著增多(P=0.003、P=0.002),視網(wǎng)膜組織水腫和空泡樣狀況改善,p-JNK、p-c-Jun、p-ERK、p-p38 MAPK和TNF-α蛋白表達(dá)明顯減少(均為P0.05),且高劑量組的改善作用更為顯著。結(jié)論白皮杉醇具有保護(hù)青光眼大鼠RGCs的作用,其作用機(jī)制可能與抑制MARK信號(hào)通路有關(guān)。
[Abstract]:Objective to observe the protective effect of taxol on retinal ganglion cells (retinal ganglion cells,RGCs) in glaucoma rats and to explore its possible mechanism. Methods Forty rats were randomly divided into control group, model group, low dose group and high dose group. The rat model of glaucoma was established by photocoagulation. The rats in the high dose group were given 100 mg kg~ (-1) and 200 mg kg~ (-1) pericycladol respectively. Intraocular pressure (IOP) was measured, RGCs was labeled with fluorescent gold retrograde and counted in each group. Retinal histopathology was observed by HE staining. Amino terminal kinase (phosphorylation c-Jun N-terminal kinase,p-JNK), phosphorylated c-Jun (phosphorylation c-junp-c-Jun), extracellular regulated protein kinase (phosphorylation extracellular regulated protein kinases,p-ERK), phosphorylated mitogen-activated protein (Jun (proto oncogene protein Jun,c-Jun), phosphorylated proto-oncogene protein (Jun (proto oncogene protein Jun,c-Jun), phosphorylated c-junp-c-Jun (phosphorylation c-junp-c-Jun), phosphorylated protein kinase (phosphorylation extracellular regulated protein kinases,p-ERK) in rat retina were detected by Western blot. Protein kinase p38 (phosphorylation mitogen activated protein kinases p-p38 MAPK and tumor necrosis factor- 偽 (tumor necrosis factor-alpha,TNF- 偽) were expressed. Results the intraocular pressure, the expression of p-JNK-c-Jun-p-ERKP p-p38 MAPK and TNF- 偽 protein in the model group were significantly higher than those in the control group (P0.05), RGCs, P0.05). Vacuoles and edema were observed in the retinal tissue structure. Compared with the model group, In the low dose group and the high dose group, the RGCs increased significantly (P0. 003 P0. 002), the retinal edema and cavitation status were improved, the expression of p-JNKP-c-Junp-ERKP-p38 MAPK and TNF- 偽 protein were significantly decreased (P0.05), and the improvement of high dose group was more significant. Conclusion Huperzine has protective effect on RGCs in glaucoma rats, and its mechanism may be related to the inhibition of MARK signaling pathway.
【作者單位】： 南陽(yáng)市中心醫(yī)院眼科;第四軍醫(yī)大學(xué)西京醫(yī)院眼科;南陽(yáng)市唐河縣城郊醫(yī)院公共衛(wèi)生服務(wù)科;
【分類號(hào)】：R775

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