Objective:To observe the inhibited effect and its mechani sm of estro gen on lightinduced apoptosis of retinal photoreceptor cells. Methods:Twenty female Sprague-Dawley rats were randomly divided into two groups: ovariectomized (OV) group and OV and estrogen (E2) replacement (OV+E2) group, with 10 rats in each group. All of the rats were exposed to the cyclic illumination under 12 hou r light and 12 hour dark condition with the light intensity of (600plusmn;35.4) lx ( a total of 14 times). All of the right eyes were extracted and the thickness of r etinal outer nuclear layer (ONL) was measured. Terminal deoxynucleotidyl Transfe rasemediated dUTP nick end labeling (TUNEL) method was used to evaluate positi v e apoptosis cells in ONL. The expression of nitric oxide synthase (NOS) in retin al cells was detected by immunohistochemistry with image analysis method. Results:The thickness of ONL in OV group was obviously thinner than that in the OV+ E2 group. The number of positive apoptosis of the cells was (0.0275plusmn;0.0069) c el ls/mu;m2 in OV group and (0.0162plusmn;0.0054) cells/mu;m2 in OV+E2group; the di fferen ce between the two groups was significant (t=4.1370，P=0.0012). The values o f in tegral optical density of NOS positively stained cells in retinal inner nuclear layer was (0.3675plusmn;0.0662) in the OV group and (0.2941plusmn;0.0350) in OV+E2 group ; the difference between the two groups was significant (t=3.4885, P=0.0031). Conclusion:Estrogen can protect retina from light injuries by regu lating NOS synthesis and inhibiting apoptosis of photoreceptor cells.
ObjectiveTo evaluate the protective effect of estrogen on survival of retinal ganglion cells (RGCs) after transient retinal ischemia-reperfusion (RIR) in rats.MethodsRIR was induced in 60 ovariectomized adult rats (OVX) by increasing intraocular pressure via an intracameral catheter. All of the rats were divided into two groups randomly: in experimental group, the rats underwent a subcutaneous injection with 17β-estrodiol（100 μg/kg） 2 hours before retinal ischemia; and in the control group, saline water was injected correspondingly. The number of RGCs and the thickness of the inner retinal layers were mesured by HE staining method before and 12, 24, 48, and 72 hours after reperfusion. TdT-mediated biotin-dUTP nick end labelling (TUNEL) staining technique was used to examine the apoptosis of RGCs.ResultsTwenty-four and 48 hours after reperfusion, the number of apoptotic cells in experimental group was obvious lower than that in the control group(Plt;0.05), and the number of RGCs in experimental group was higher than that in the control group(Plt;0.05).ConclusionEstrogen can protect retinal neurons from transient RIR in ovariectomized rats.(Chin J Ocul Fundus Dis, 2005,21:177-179)
ObjectiveTo study the etiology and clinical features of patients with ophthalmoplegia resulting in vertigo. MethodsWe retrospectively analyzed the clinical data of 45 patients with vertigo caused by ophthamloplegia treated between January 2010 and December 2013. The causes and features of the disease, treatment and outcome were summarized. ResultsAmong the factors responsible for ophthalmoplegia resulting in vertigo, myasthenia gravis (MG) took the first place (20/45, 44.4%), followed by Graves' ophthalmopathy (9/45, 20.0%), diabetes (5/45, 11.1%), intracranial infection (4/45, 8.9%), medial rectus injury (3/45, 6.7%), orbital tumor (2/45, 4.4%), and Lambert-Eaton Myasthenic Syndrome (2/45, 4.4%). In 36 patients, the lesions located in the neuromuscular junction or muscles (80.0%). The pathogenesis of ophthalmoplegia were almost all caused by systemic diseases (88.9%), and the occurrence of local ophthalmology diseases was fewer (11.1%). Etiological treatments achieved beneficial effects. ConclusionThe etiology of ophthalmology diseases resulting in vertigo is confusing. We should care more for patients with ophthalmoplegia caused by systemic diseases resulting in ophthalmologic vertigo without vision damage. Careful examinations and proper treatments for etiological factors are necessary in clinical options.