Anti-VEGF reduces inflammatory features in macular edema secondary to retinal vein occlusion.

AIM: To investigate the anti-inflammatory effect of intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF) in patients with macular edema secondary to retinal vein occlusion (RVO-ME). METHODS: Twenty-eight eyes from twenty-eight treatment-naïve patients (14 males and 14 females) with RVO-ME were included in this retrospective study. The retinal vein occlusion (RVO) was comprised of both central retinal vein occlusion (CRVO, n=14) and branch retinal vein occlusion (BRVO, n=14). Intravitreal injection of anti-VEGF reagents were administered monthly for three consecutive months, in which 18 patients were injected with ranibizumab and 10 patients were injected with conbercept. All eyes were imaged with optical coherence tomography angiography (OCTA) at baseline and 1wk after monthly intravitreal anti-VEGF injection. The visual acuity (VA), central macular thickness (CMT), the number of hyperreflective foci (HRF) recognized as an inflammatory sign in OCT images, and non-perfusion area (NPA), were compared before and after anti-VEGF treatments. RESULTS: The mean interval between baseline and follow-up was 29.4±0.79 (range, 27-48)d. Compared with the baseline, the VA improved (logMAR 1.5±0.1 vs 0.8±0.1, P<0.05) and CMT decreased (460±34.0 µm vs 268.8±12.0 µm, P<0.05), significantly, after anti-VEGF treatment. The number of HRF was decreased significantly (76.5±4.8 vs 47.8±4.3, P<0.05) after anti-VEGF treatment. CONCLUSION: Anti-VEGF therapy is effective in treating RVO-ME. The mechanisms for the decreased HRF and the reduction of NPA by anti-VEGF therapy merits further exploration.

A novel surgical technique of internal limiting membrane peeling for high myopic foveoschisis: a wide range of whole piece consecutive peeling without preservation of epi-fovea.

AIM: To demonstrate an improved surgical technique of whole piece consecutive internal limiting membrane (ILM) peeling without preservation of the epi-fovea to treat high myopic foveoschisis (MF). METHODS: A 23-gauge 3-port pars plana vitrectomy was performed on 16 patients with high MF. A parallel arc line along the vascular arcades was scraped out with a curved membrane scraper DSP. Next, an ILM forceps was used to catch hold of the incisal edge of the ILM flap, and the action of releasing and separating was subsequently taken toward the direction of the macular fovea. Next, the ILM forceps was used to grasp the released area, and the whole area coherent ILM peeling covering the macular fovea was implemented thereafter. Finally, the ILM was folded backwards and peeled off in the arc direction. RESULTS: At the final visit, the average central macular thickness decreased remarkably from 423.76±177.67 to 178.24±66.21 µm. The mean logarithm of the minimum angle of resolution best-corrected visual acuity of 1.37±0.59 was significantly alleviated to 0.74±0.59. CONCLUSION: The wide range of whole piece consecutive ILM peeling without preservation of the epi-fovea is proven to be effective and significantly reduced the occurrence of retinal tear and macular hole.

Lutein supplementation improves visual performance in Chinese drivers: 1-year randomized, double-blind, placebo-controlled study.

OBJECTIVES: Although it is known that the carotenoid lutein can affect visual performance, we still have much to learn about its effect in occupational populations, like drivers. The aim of this study was to examine the effect of lutein supplementation on visual function in healthy drivers with long-term light exposure. METHODS: The study was a randomized, double-blind, placebo-controlled, 1-y intervention study. It included 120 normal participants (drivers). The active (A) group consumed 20 mg of lutein daily. Participants were assessed at baseline, 1, 3, 6, and 12 mo (V0, V1, V2, V3, and V4, respectively). Assessment included visual acuity, serum lutein concentrations, macular pigment optical density (MPOD), and visual performance. At the onset and at the end of the intervention, dietary intakes of lutein and visual-related quality of life were measured. RESULTS: There was a trend (in the active group) toward an increase in best spectacle-corrected visual acuity measured, but there were no significant differences. Serum lutein and central MPOD in the active group increased significantly, whereas no change was observed in the placebo group. We observed significant increases in contrast and glare sensitivity, especially in the mesopic condition. There were significant improvements in the score of the National Eye Institute 25-Item Visual Functioning Questionnaire driving subscale in the active group. CONCLUSIONS: Daily supplementation with 20 mg of lutein increases MPOD levels. Lutein may benefit driving at night and other spatial discrimination tasks carried out under low illumination.

Effects of estrogen on collagen gel contraction by human retinal glial cells.

BACKGROUND: There are definite gender differences in patients with macular holes. Menopausal women over 50 years are most affected. We aimed to observe the effect of estrogen on collagen gel contraction by cultured human retinal glial cells. It is speculated that estrogen could strengthen the tensile stress of the macula by maintaining the correct morphology and contraction. METHODS: Estrogen was used to determine its effects on collagen gel contraction, and its function was measured using morphological changes in cells. Human retinal glial cells were cultured in collagen solution. The cells were then exposed to collagen gels and the degree of contraction of the gel was determined. RESULTS: Estrogen at differing concentrations had no effect on the growth of human retinal glial cells. However, after exposed to collagen gel block, less contraction was noted in the estrogen-treated group than in the control group. CONCLUSIONS: Estrogen can inhibit collagen gel contraction by glial cells. These results suggest a mechanism for macular hole formation, which is observed in menopausal females.

EGB761 on retinal light injury in rats.

BACKGROUND: Retinal light injury can lead to degeneration of the photoreceptor cell layer. It has been hypothesized that the mechanism for this process is the photochemical damage. Ginkgo balboa extract (Ginkgo biloba extract EGB761) EGB761 is a free radical scavenger. The purpose of this study was to investigate the possible effect of orally administered EGB761 on retinal light damage of mouse photoreceptor cells. METHODS: Kunming mice were randomly chosen for the following groups containing 20 animals in each: control group, light damage group, saline control group, and drug treatment group. The drug treatment group and saline control group were given daily gavage of EGB761 (150 mg×kg(-1)×d(-1)) one week before light exposure. At 7, 14, and 30 days after light exposure, animals were sacrificed and eyes were examined by light microscopy, electron microscopy, and retinal histopathology using in situ detection of apoptotic cells. RESULTS: In the light damage group after 7 days there was visible edema, and the outer nuclear layer appeared withered with deeply stained dead cells, leaving only a thin nuclear layer of 7 - 8 cells. After 14 days, the photoreceptor cell layer disappeared, leaving only the outer nuclear layer of 1 - 3 cells with an average thickness of (37.988 ± 1.207) µm. The average thickness of the retina was (126.32 ± 2.31) µm. In the drug treatment group, the photoreceptor cell layer and outer nuclear layer damage were significantly lower than the saline group (t = 21.993, P < 0.001), demonstrating that EGB761, especially at 14 days after light exposure, can reduce retinal light damage in mice. CONCLUSION: Oral administration of EGB761 can partially inhibit apoptosis of photoreceptor cells, resulting in increased photoreceptor cell survival.

[Chinese herbal medicine Lingqi Huangban Granule protects retinal pigment epithelial cells against oxidative stress-induced injury in vitro].

OBJECTIVE: To observe the protective effects of drug-contained serum of Lingqi Huangban Granule (LQHBG), a compound traditional Chinese herbal medicine, on oxidative stress-induced injury in rabbit retinal pigment epithelial (RPE) cells in vitro. METHODS: The oxidative stress of rabbit RPE cells in vitro was induced with hydrogen peroxide (500µmol/L) and different concentrations of LQHBG were administered to rats to prepare medicated serum. RPE cells were randomized into normal control group (no hydrogen peroxide), model group (hydrogen peroxide), model plus serum group (hydrogen peroxide and 10% control serum), model plus low-dose LQHBG group (hydrogen peroxide and low-dose LQHBG-medicated serum) and model plus high-dose LQHBG group (hydrogen peroxide and high-dose LQHBG-medicated serum). Teminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assay and flow cytometry (FCM) were used to measure apoptosis of cultured rabbit RPE cells. Protein expressions of caspase-3 and Bcl-X(L) were observed by Western blot method. RESULTS: FCM results showed that the apoptotic rates of the normal control group, model group, control serum group and serum containing low- and high-dose LQHBG groups were (4.85±0.26)%, (20.02±1.37)%, (21.84±0.94)%, (13.56±0.55)%, and (8.58±0.39)%, respectively; compared with the model group, the apoptotic rates of RPE cells in the low- and high-dose LQHBG groups were obviously reduced in a dose-related manner (P<0.05). TUNEL results showed that nuclei of apoptotic cells were stained brown; the number of apoptotic cells in the low- and high-dose LQHBG groups was obviously less than that in the model group. The protein expression of caspase-3 was up-regulated in the model and control serum groups, which was higher than that in the high-dose LQHBG group (P<0.05). The protein expression of Bcl-X(L) was down-regulated in the model and control serum groups, which was lower than that in the low- and high-dose LQHBG groups (P<0.01). CONCLUSION: Drug-contained serum of LQHBG obviously reduces apoptosis and partly protects rabbit RPE cells from oxidative stress-induced injury. The protective function is due to an improvement in antioxidant abilities, down-regulation of the expression of caspase-3 and up-regulation of the expression of Bcl-X(L).

[Kininogen-1 and insulin-like growth factor binding protein-6 as serum biomarkers for proliferative vitreoretinopathy].

OBJECTIVE: To evaluated the predictive potential of kininogen-1 and insulin-like growth factor binding protein-6 (IGFBP-6) for PVR. METHODS: Vitreous and serum samples were obtained from 24 PVR patients. Vitreous from 8 donated normal eyes, and serum samples from 20 healthy volunteers served as control. Patients who underwent vitrectomy with C(3)F(8) gas tamponade (n = 15) and silicone tamponade (n = 8) and patients who experienced recurrent retinal detachment after scleral buckling surgery (n = 8) were recruited for serum tests as well. Western blot analysis was employed to detect the presence of kininogen-1 and IGFBP-6. The protein concentration was measured by using enzyme linked immunosorbent assay (ELISA) analysis. All date were analyzed with the SPSS 3.0 for Windows (only-way analysis of variance and t test). RESULTS: Western blot analysis displayed that except that IGFBP-6 was absent in 2 PVR vitreous, both kininogen-1 and IGFBP-6 were otherwise found in all PVR vitreous and serum samples. Neither kininogen-1 nor IGFBP-6 can be detected in normal vitreous or serum samples. Protein expression was more intensive in severe PVR vitreous than in mild PVR vitreous, which was confirmed by a significantly higher concentration of each protein in sever PVR vitreous. The ELISA outcomes documented that kininogen-1 concentration in vitreous were significantly higher in severe PVR patients than those in mild PVR (281.0 ± 63.0 & 237.5 ± 32.1) µg/L (t = 5.44, P < 0.05). Kininogen-1 was about 2 times higher in serum than in vitreous (443.3 ± 190.1) µg/L (t = 5.27, P < 0.05). At 6 months after vitrectomy with gas tamponade in 15 patients, their kininogen-1 level in serum was significantly lower than that of preoperation (81.9 ± 18.6 & 443.3 ± 190.1) µg/L (t = 5.26, P < 0.05) and encircling failure group was (116.8 ± 45.1) µg/L, it was higher than that of normal and silicone tamponade groups (t = 3.95, 4.34;P < 0.05). Similarly, IGFBP-6 concentration in vitreous were significantly higher in severe PVR patients than those in mild PVR (352.9 ± 64.4 & 283.9 ± 69.9) ng/L (t = 5.08, P < 0.05) and its level in serum was (185.3 ± 34.9) ng/L and lower than that of in vitreous(t = 7.95, P < 0.05). At 6 months after vitrectomy with gas tamponade in 15 patients, their IGFBP-6 level in serum decreased comparing that of preoperation (65.4 ± 31.8) ng/L (t = 11.10, P < 0.05) and encircling failure group was (109.2 ± 6.6) ng/L, it was higher than that of normal and silicone tamponade groups (t = 3.16, 2.77; P < 0.05). CONCLUSIONS: Kininogen-1 and IGFBP-6 are presented in serum and vitreous in PVR patients. The strength of protein expression is related to the severity of PVR. These results suggested that kininogen-1 and IGFBP-6 can be biomarkers for severe PVR.