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Objective To determine the difference of global indices of retinal thickness at posterior pole in primary and suspected glaucoma. Methods Forty five global indices of analysis on retinal thickness at posterior pole in every case, including 12 cases of primary open angle glaucoma and 11 cases of suspected glaucoma were obtained by advanced retinal thickness analyzer. Every index was also compared. Results There were significant differences between primary and suspected glaucoma in foveal shape deviation (FSD), foveal corrected thickness deviation (FCTD), foveal fixation corrected thickness deviation (FFD), foveola thickness deviation (VTD), corrected foveola thickness deviation (CVTD), peri foveal abnormally thin area (PFATN), posterior pole pattern deviation (PPPD), and posterior pole abnormally thin area (PPATN). Conclusion There are significant difference of morphologic indices of retinal thickness at posterior pole between primary and suspected glaucoma.
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Objective To investigate the expression of induced heat shock protein (HSP) 70 in rat′s retinal neurons (RNs) and M?ller cells, and evaluate the protective effect of HSP 70 on RNs injured with glucose deprivation and glutamate. Methods Rat′s RNs and M?ller cells cultured in vitro were treated with heat shock (42℃ for 1 hour), and duration of the expression of HSP70 was detected by immunocytochemical techniques. Viability of the cells was measured by methyl thiazolyl tetrazolium (MTT) chromatometry after incitant toxic injury with glucose deprivation (0.56 mmol/L glucose for 6 hours) and glutamate (100 ?mol/L for 6 hours). Simultaneously, the expression was interdicted by HSP70. Results Hypereffective expression of HSP70 was found in cultured RNs and M?ller cells after heat shock. The viability of RNs pretreated by heat shock after injured with glucose deprivation and glutamate significantly increased which could be interdicted by HSP70 antibody. Conclusion Hypereffective expression of HSP 70 may be induced by heat shock, which enhances the ability of tolerance of RNs to the incitant toxic injury by glucose deprivation and exitotoxicity.
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Objective To detect the induction of inducible nitric oxide synthase (iNOS) and nitric oxide (NO) production in immunostimulated retinal pigment epithelial (RPE) cells to seek for the supplying of the arginine, a substrate for NOS; as well as the effects of produced NO on the tight junction of RPE-J cells. Methods Rat′s RPE-J cells were treated with interferon-?(INF-?), tumor necrosis factor-?(TNF-?) and lipopolysaccharide (LPS), and Northern and Western blotting were applied to analyze the expression of the citrulline-NO cycle enzymes and related enzymes and the effect of dexamethasone and cyclic adenosine monophosphate (camp) on the expression of iNOS. Immunocytochemistry reaction and Western blotting were used to evaluate the effect of produced NO on the tight junctions of RPE-J cells. Results iNOS and argininosuccinate synthetase (AS) were highly induced at both mRNA and protection levels in immunostimulated RPE cells while arginiosuccinate lyase (AL) was not induced. NO was produced by cells after stimulation with TNF?, IFN? and LPS. The induction of iNOS mRNA and the production of NO by these immunostimulated cells was further enhanced by cAMP. NO was produced from citrulline as well as from arginine. And the produced NO impaired the tight junction of RPE-J cells, decreased the production of tight junction related protein ZO-1. Conclusion In activated RPE-J cells, citrulline-arginine recycling is important for NO production, and the produced NO weakened the function of tight junction of RPE-J cells.