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黄芪多糖对高眼压大鼠视网膜神经节细胞凋亡的影响 被引量:9

Effect of astragalus polysaccharide on the apoptosis of retinal ganglion cells of ocular hypertension rats
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摘要 目的研究黄芪多糖对高眼压大鼠视网膜神经节细胞凋亡及磷脂酰肌醇-3-激酶/丝苏氨酸蛋白激酶(PI3K/AKT)通路的影响。方法将24只眼压正常大鼠以烧灼巩膜上静脉法构建高眼压模型大鼠,并随机分为模型组与实验组,各12只;另选10只眼压正常SD大鼠为对照组。建模1周后实验组大鼠灌服500 mg·kg^-1黄芪多糖,模型组与对照组大鼠则灌服等量生理盐水,连续干预2周。以苏木精-伊红(HE)染色观察视网膜组织病理学形态变化及各层厚度;以原位末端标记法(TUNEL)检测视网膜组织视网膜神经节细胞凋亡;以蛋白质印迹(Wb)法检测视网膜组织PI3K/AKT通路相关蛋白表达。结果对照组、模型组、实验组大鼠视网膜全层厚度分别为(162.35±10.09),(274.19±13.64),(201.22±12.11)μm;内颗粒层厚度分别为(23.97±2.21),(51.02±3.45),(40.23±3.03)μm;外颗粒层厚度分别为(49.87±3.12),(103.52±9.85),(81.24±7.66)μm;视神经纤维层厚度分别为(33.17±2.96),(69.08±4.23),(51.29±3.50)μm;视网膜神经节细胞凋亡指数分别为(1.02±0.03)%,(23.45±2.01)%,(2.17±1.01)%。模型组大鼠视网膜全层、内颗粒层、外颗粒层、视神经纤维层厚度及视网膜神经节细胞凋亡指数均较对照组显著升高,而实验组较模型组降低;模型组大鼠视网膜组织p-PI3K、p-AKT蛋白相对表达量较对照组降低,而实验组较模型组升高,差异均有统计学意义(均P<0.05)。结论黄芪多糖可有效抑制高眼压大鼠模型视网膜神经节细胞凋亡,缓解视网膜组织病变,其作用机制可能与抑制PI3K/AKT通路信号转导相关。 Objective To explore the effect of astragalus polysaccharide on the apoptosis of retinal ganglion cells and phosphatidyl inositol-3-kinase/silk/threonine protein kinase(PI3 K/AKT)pathways of hypertensive rats.Methods Twenty-four intraocular pressure normal rats were built hypertensive rat model by burning sclera vein method,and they were divided randomly into model group and test group,12 rats in each group;another 10 intraocular pressure normal rats were selected as control group.After 1 week modeling,the rats in test group were gastrointestinal administrated 500 mg·kg^-1 astragalus polysaccharide,and rats in model group and control group were gastrointestinal administrated the same amount of saline,all were intervened for continuous 2 weeks.The retinal tissue pathology shape change and thickness of each layer were observed by hematoxylin and eosin(HE)staining,the apoptosis of retinal tissue retinal ganglion cells were detected by terminal deoxynucleotidyl transferase dUTP nick-end labeling(TUNEL);the PI3 K/AKT pathways related proteins expression in retinal tissue were detected by Western blot(Wb).Results The retinal thickness in control group,model group and test group were(162.35±10.09),(274.19±13.64),(201.22±12.11)μm respectively;the inner plexiform thickness were(23.97±2.21),(51.02±3.45),(40.23±3.03)μm;the outer plexiform thickness were(49.87±3.12),(103.52±9.85),(81.24±7.66)μm;the retinal nerve fiber layer thickness were(33.17±2.96),(69.08±4.23),(51.29±3.50)μm;the retinal ganglion cell apoptosis indexes were(1.02±0.03)%,(23.45±2.01)%,(2.17±1.01)%.The retinal thickness,inner plexiform thickness,outer plexiform thickness,retinal nerve fiber layer thickness and retinal ganglion cell apoptosis index in model group increased compared with control group,while test group decreased compared with model group;the p-PI3 K,p-AKT protein relative expression in retinal tissue of rats in model group decreased compared with control group,while test group increased compared with model group,the difference were all had statistical significance(all P<0.05).Conclusion Astragalus polysaccharide can inhibit the apoptosis of retinal ganglion cells of hypertensive rats,relieve retinal tissue lesions,and the action mechanism may be related to the inhibition of PI3 K/AKT pathway signal transduction.
作者 彭涛 于丹丹 谢美娜 何洁云 PENG Tao;YU Dan-dan;XIE Mei-na;HE Jie-yun(Department of Ophthalmology,China Coast Guard Hospital of the People’s Armed Police Force,Jiaxing 314000,Zhejiang Province,China)
出处 《中国临床药理学杂志》 CAS CSCD 北大核心 2020年第10期1344-1346,共3页 The Chinese Journal of Clinical Pharmacology
基金 嘉兴市科技计划基金资助项目(2017AY33063)。
关键词 高眼压 视网膜神经节细胞 凋亡 磷脂酰肌醇-3-激酶/丝苏氨酸蛋白激酶通路 ocular hypertension retinal ganglion cell apoptosis phosphatidyl inositol-3-kinase/silk/threonine protein kinase pathway
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