Publications by authors named "Dianwen Gao"

Aim: To study the gene expression response and predict the network in cell due to pressure effects on optic nerve injury of glaucoma.

Methods: We used glaucoma related microarray data in public database [Gene Expression Omnibus (GEO)] to explore the potential gene expression changes as well as correspondent biological process alterations due to increased pressure in astrocytes during glaucoma development.

Results: A total of six genes were identified to be related with pressure increasing.

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This study aimed to investigate the impacts of erythropoietin (EPO) on the electroretinogram b‑wave (ERG‑b), and on the mRNA and protein expression levels of hypoxia‑inducible factor‑1α (HIF‑1α), inducible nitric oxide synthase (iNOS), cyclooxygenase‑2 (COX‑2) and caspase‑9 in chronic ocular hypertension rats. Episcleral vein cauterization (EVC) was used to establish the chronic ocular hypertension rat model based on the intraocular pressure (IOP) value. ERG‑b and mRNA and protein expression levels of HIF‑1α, iNOS, COX‑2 and caspase‑9 in normal, EVC‑treated and EVC combined with EPO (EVC+EPO)‑treated rats were measured by electroretinography, RT‑PCR and western blotting, respectively.

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A plasmid for cytoglobin expression, pAcGFP1-C1-cytoglobin, was transfected into SH-SY5Y cells. Cobalt chloride was used to establish a model of hypoxia. Western blotting indicated that cytoglobin was overexpressed and there was low expression of hypoxia-inducible factor-1α in SH-SY5Y cells after transfection.

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The aim of this study was to determine the effect of the EphB4 monoclonal antibody on experimental choroidal neovascularization (CNV) progression. Experimental CNV was established by argon laser photocoagulation. In the experimental group, the EphB4 monoclonal antibody was injected into the vitreous space in the eye specimens on days 0, 3, 6 and 9 after CNV model establishment.

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Some ocular diseases characterized by apoptotic death of retinal ganglion cells (RGCs) and Alzheimer's disease (AD) are chronic neurodegenerative disorders and have similarities in neuropathology. Humanin (HN) is known for its ability to suppress neuronal death induced by AD-related insults. In present study, we investigated the neuroprotective effects of HN on hypoxia-induced toxicity in RGC-5 cells.

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Abnormal activation of Rho kinase (ROCK) plays a vital role in the pathogenesis of ischemia/reperfusion (I/R)-induced retinal injury. The aim of this study was to investigate whether fasudil, a potent inhibitor of ROCK, has a protective effect on retinal I/R injury in rats and to explore the possible underlying mechanisms. Forty adult Sprague-Dawley rats were randomly assigned into sham, I/R injury model (I/R), model plus normal saline (control), and model plus fasudil (fasudil) groups.

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Aim: To investigate the anti-apoptotic effect of transforming growth factor beta-1 (TGF-β(1)) on chronic ocular hypertension.

Methods: The expression of TGF-β(1) in retinal ganglion cells (RCGs) was measured using the immunohistochemiscal S-P method and real-time PCR in the normally control group, the ocular hypertension group (experimental group A), the ocular hypertension plus antibody intervention group (experimental group B) and the ocular hypertension plus antigen intervention group (experimental group C) at 1, 2, 3 and 4 weeks postoperatively. The count of apoptotic RCGs was measured using the TUNEL method.

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Aim: To investigate the effect of aminoguanidine (AG) on the expression of caspase-3 in rat retina after ischemia- reperfusion injury.

Methods: The rats were anesthetized with 30mg/kg sodium pentobarbital introperitoneal(ip) injections. After topical application of 10g/L dicaine, the anterior chamber was punctured with a 5-gauge needle connected to a bottle containing normal saline.

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Aim: To estimate the effects of human umbilical vein (HUV) implanted under the sclera of glaucoma model on intraocular pressure (IOP) lowering and to investigate its related mechanisms

Methods: A total of 20 human umbilical veins (HUV) were collected from healthy fetus umbilical core. After the establishment of glaucoma model in rabbits, human freeze-dried umbilical vein was implanted under the sclera during NPDS, while for control group, sclerostomy was performed without implant. The formation of the filtration bleb and IOP were detected every 24 hours before surgery and on day 3, 7, 10 and 14 after surgery.

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Aim: To research the effect of erythropoietin (EPO) to the HIF-1\iNOS signal transduction path in retina in chronic ocular hypertension rat.

Methods: One hundred and twenty Wistar rats were divided into 12 groups randomly. Two episcleral veins were coagulated unilaterally in rats with electric coagulator to establish the glaucoma model.

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Aim: To study the expressive variation of Nogo-A on rat retina in the process of chronic ocular hypertension.

Methods: Thirty-six healthy adult male Wistars were randomly divided into control group (6 rats) and chronic hypertension group (30 rats). Chronic hypertension was created by cauterizing the superficial scleral veins.

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Purpose: To observe the expression of extracellular matrix in cornea and its relationship with corneal opacity after epithelial ingrowth in LASIK.

Methods: Corneal flap was made on rabbit eyes, and epithelial cells mechanically scraped from surroundings the flap were implanted underneath. The corneas were harvested 1, 3, 7 and 30 days following surgery, histological and immunohistochemical examination was performed.

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Objective: To investigate the results and technology of making corneal flaps with Moria M(2) microkeratome.

Methods: Eight hundred and six corneal flaps (in 409 cases) were made using Moria M(2) microkeratome in LASIK. The group consisted of 205 males (405 eyes), whose mean age was (23.

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Objective: To investigate the role of interleukin-10 (IL-10) in herpetic stromal keratitis (HSK).

Methods: Eighty BALB/c mice were divided into two groups and infected with HSV-1 Mckrae strain by corneal scarification. Murine rIL-10 (20 ng/ml) was inoculated intracorneally 6 h before and again on days 0, 2 and 4 after topical HSV-1 corneal infection.

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