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find Author "胡健艳" 4 results
  • 植入用氟尿嘧啶缓释剂抑制增生性玻璃体视网膜病变

    Release date:2016-09-02 05:51 Export PDF Favorites Scan
  • 丝裂原活化蛋白激酶信号通路与眼底新生血管性疾病相关性的研究进展

    丝裂原活化蛋白激酶(MAPK)信号通路中主要存在3种亚型,分别为细胞外信号调节激酶(ERK)、c-Jun氨基末端激酶(JNK)和p38 MAPK。它们在各亚群内部均存在着类似的、相互独立的三级级联反应,在适当刺激因素下作用于不同的底物可产生不同的细胞生物学效应。眼底新生血管是多种致盲眼病的病理基础,是多种因子相互作用导致促血管生成因子和抗血管生成因子间的平衡失调的结果;而有关多种因子发挥生物效应的MAPK信号通路在眼底新生血管发生发展过程中的作用越来越引起注意。MAPK信号通路在糖尿病视网膜病变、早产儿视网膜病变、老年性黄斑变性、视网膜静脉阻塞等疾病的新生血管形成中发挥重要的调控作用。通过对MAPK信号通路在眼底新生血管作用机制的探索,有助于深入详尽地了解眼部疾病的形成和发展规律,为预防和控制眼底新生血管形成和发展提供新的思路和方案。在未来,针对MAPK信号通路的靶向治疗将成为有效抑制眼底新生血管形成的重要治疗方案之一。

    Release date:2016-09-02 05:22 Export PDF Favorites Scan
  • The effects and mechanisms of G protein-coupled receptor 91 on blood-retinal barrier in diabetic rats

    ObjectiveTo investigate the effects and mechanisms of G protein-coupled receptor 91 (GPR91) on blood-retinal barrier (BRB) in diabetic rats. MethodsA lentiviral vector of shRNA targeting rat GPR91 and scrambled shRNA were constructed. Healthy male Sprague-Dawley (SD) rats were selected in this study. The 60 rats were randomized into 4 groups and treated as follows:(1) control group (Group A, n=15), the rats received injections of an equal volume of 0.1% citrate buffer; (2) streptozocin (STZ) group (Group B, n=15), the rats received injections of STZ; (3) LV.shScrambled group (Group C, n=15), diabetic rats received an intravitreal injection of 1 μl 1×108 TU/ml scrambled shRNA lentiviral particles at 2 weeks after the induction of diabetes; (4) LV.shGPR91 group (Group D, n=15), diabetic rats received an intravitreal injection of 1 μl 1×108 TU/ml pGCSIL-GFP-shGPR91 lentiviral particles. At 12 weeks after intravitreal injection, immunohistochemistry and Western blot were used to assess the expression of GPR91, p-extracellular signal-regulated kinase(ERK)1/2, t-ERK1/2, p-Jun N-terminal kinase (JNK), t-JNK, p-p38 mitogen-activated protein kinase (MAPK) and t-p38 MAPK. Haematoxylin and eosin (HE) staining and Evans blue dye were used to assess the structure and function of the retinal vessel. Immunohistochemistry enzyme-linked immunosorbent assay (ELISA) was used to test the protein level of VEGF. ResultsImmunohistochemistry staining showed that GPR91 was predominantly localized to the cell bodies of the ganglion cell layer. Western blot showed that GPR91 expression in Group D decreased significantly compared with Group C (F=39.31, P < 0.01). HE staining showed that the retina tissue in Group B and C developed telangiectatic vessels in the inner layer of retina, while the telangiectatic vessels attenuated in Group D. It was also demonstrated in Evans blue dye that the microvascular leakage in Group D decreased by (33.8±4.11)% compared with Group C and there was significant difference (F=30.35, P < 0.05). The results of ELISA showed the VEGF secretion of Group B and C increased compared with Group A and the VEGF expression in Group D was significantly down regulated after silencing GPR91 gene (F=253.15, P < 0.05).The results of Western blot indicated that compared with Group A, the expressions of p-ERK1/2, p-JNK and p-p38 MAPK were significantly upregulated (q=6.38, 2.94, 3.45;P < 0.05). Meanwhile, the activation of ERK1/2 was inhibited by GPR91 shRNA and the difference was statistically significant (F=22.50, P < 0.05). ConclusionsThe intravitreal injection of GPR91 shRNA attenuated the leakage of BRB in diabetic rats. GPR91 regulated the VEGF release and the leakage of BRB possibly through the ERK1/2 signaling pathway.

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  • The current status and progress of the pathological changes and related molecular mechanisms of neuroretinal injury in diabetic retinopathy

    The neuroretinal injuries of diabetic retinopathy (DR) include retinal neuronal damage and reactive gliosis, both of which are induced by hyperglycemia and presented as early features of DR. They promote to develop mutually and accelerate the progression of DR. The molecular mechanisms study of neuronal damage mainly focuses on the alterations of extracellular environment and related signaling pathways, include inflammation, oxidative stress, endoplasmic reticulum stress, the formation of advanced glycation end products, glutamate toxicity and so on. These alterations mainly result in neuronal apoptosis and autophagy. The damaged neurons activate the glial cells with apparent changes in morphology, cell counts and the level of intracellular protein expression. In non-proliferative DR, glial cells are moderately hypertrophic and slightly increased in numbers. In proliferative DR, there is a significant rise in glial cell number with enhanced level of inflammatory factors and vascular active substances which lead a further neuronal damage. Signaling pathways of extracellular signal-regulated kinase 1/2, c-Fos and p38 mitogen-activated protein kinase are associated with their activation. Researches on the molecular mechanisms and signaling pathways of the DR will promote controlling the DR progression at the cellular level.

    Release date:2017-05-15 12:38 Export PDF Favorites Scan
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