Oxygen Saturation in Closed-Globe Blunt Ocular Trauma

. Purpose. To evaluate the oxygen saturation in retinal blood vessels in patients after closed-globe blunt ocular trauma. Design. Retrospective observational case series. Methods. Retinal oximetry was performed in both eyes of 29 patients with unilateral closedglobe blunt ocular trauma. Arterial oxygen saturation (SaO 2 ), venous oxygen saturation (SvO 2 ), arteriovenous difference in oxygen saturation (SO 2 ), arteriolar diameter, venular diameter, and arteriovenous difference in diameter were measured. Association parameters including age, finger pulse oximetry, systolic pressure, diastolic pressure, and heart rate were analyzed. Results. The mean SaO 2 in traumatic eyes (98.1% ± 6.8%) was not significantly different from SaO 2 in unaffected ones (95.3% ± 7.2%) ( = 0.136). Mean SvO 2 in traumatic eyes (57.1% ± 10.6%) was significantly lower than in unaffected ones (62.3% ± 8.4%) ( = 0.044). The arteriovenous difference in SO 2 in traumatic eyes (41.0% ± 11.2%) was significantly larger than in unaffected ones (33.0% ± 6.9%) ( = 0.002). No significant difference was observed between traumatic eyes and unaffected ones in arteriolar ( = 0.249) and venular diameter ( = 0.972) as well as arteriovenous difference in diameter ( = 0.275). Conclusions. Oxygen consumption is increased in eyes after cgBOT, associated with lower SvO 2 and enlarged arteriovenous difference in SO 2 but not with changes in diameter of retinal vessels

PTEN Reduced UVB-Mediated Apoptosis in Retinal Pigment Epithelium Cells

Age-related macular degeneration (AMD) is a leading cause of blindness and progressive loss of central vision in the elderly population. The important factor of AMD pathogenesis is the degeneration of retinal pigment epithelial (RPE) cells by oxidative stress. Inactivation of PTEN can disrupt intercellular adhesion in the RPE cells, but the mechanism of oxidative stress is less known. Here we presented evidence that UVB-mediated oxidative stress induced apoptosis in ARPE-19 cells. Downregulation of the expression of PTEN in UVB-irradiative RPE cells triggered DNA damage and increased the level of UVB-induced apoptosis by activating p53-dependent pathway. However, overexpression of PTEN increased cell survival by suppressing p-H2A in response to DNA damage and apoptosis. When using Pifithrin-α (one of p53 inhibitors), the level of p53-dependent apoptosis was significantly lower than untreated, which suggested that p53 was possibly involved in PTEN-dependent apoptosis. Thus, it elucidated the molecular mechanisms of UVB-induced damage in RPE cells and may offer an alternative therapeutic target in dry AMD

Curcumin Inhibits Proliferation and Epithelial-Mesenchymal Transition in Lens Epithelial Cells through Multiple Pathways

Background. Posterior capsule opacification (PCO), a complication of extracapsular lens extraction surgery that causes visual impairment, is characterized by aberrant proliferation and epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Curcumin, exerting inhibitive effects on cell proliferation and EMT in cancer, serves as a possible antidote towards PCO. Methods. Cellular proliferation of LECs after treatment of curcumin was measured with MTT assay and flow cytometry. The transcriptional and expressional levels of proteins related to proliferation and EMT of LECs were quantified by western blotting and real-time PCR. Results. Curcumin was found to suppress the proliferation of LECs by inducing G2/M arrest via possible inhibition of cell cycle-related proteins including CDK1, cyclin B1, and CDC25C. It had also inactivated proliferation pathways involving ERK1/2 and Akt pathways in LECs. On the other hand, curcumin downregulated the EMT of LECs through blocking the TGF-β/Smad pathway and interfering Notch pathway which play important roles in PCO. Conclusions. This study shows that curcumin could suppress the proliferation and EMT in LECs, and it might be a potential therapeutic protection against visual loss induced by PCO