Age-related macular degeneration (AMD) involves dysregulation of the innate immune response of complement and mononuclear phagocytes and abnormalities of local microglia. When microglia transition from a resting state to an active state, their metabolic pathway also changes, known as "metabolic reprogramming", and their glucose metabolic reprogramming is a key factor in the pathogenesis of AMD, involving multiple signaling pathways. Including phosphatidylinositol 3-kinase-serine threonine kinase-rapamycin target, adenylate activated protein kinase and hypoxia-inducing factor 1 pathway. These metabolic changes regulate the inflammatory response, energy supply, and neuroprotective functions of microglia. Therapeutic strategies to regulate the reprogramming of glucose metabolism in microglia have achieved initial results. Future studies should further explore the mechanisms of microglia metabolic regulation to develop new targeted drugs and intervene in the treatment of AMD through anti-cellular aging pathways.
Objective To observe the macular structure changes and its relationship with visual function in patients with idiopathic macular hole (IMH). Methods Forty-seven patients (47 eyes) with IMH who underwent pars plana vitrectomy were enrolled in this study. All patients were examined including bestcorrected visual acuity (BCVA), slit-lamp microscopy, indirect ophthalmoscopy, B-scan ultrasonography, optical coherence tomography (OCT) and MP-1. All the patients underwent a standard three-port pars plana vitrectomy. The BCVA, mean light sensitivity (MS) in macular area, macular hole diameter, the photoreceptor inner and outer segment (IS/OS) junction defect, external limiting membrane (ELM) defect were observed on the 1st, 3rd and 6th months after surgery, and then the relationship of IS/OS junction defect, ELM defect, sensitive and BCVA were analyzed. Results The 1st, 3rd and 6th months after surgery, the logarithm of minimal angle of resolution (logMAR) BCVA (t=16.4, 35.7, 20.7; P＜0.05) and MS （t=－13.8, －17.9, －2.5; P＜0.05） were improved significantly; the macular hole diameter （t=7.7, 7.7, 7.7;P＜0.05）, IS/OS junction defect （t=24.1, 19.3, 27.4; P＜0.05） and ELM （t=20.5, 6.7, 15. 8; P＜0.05） defect were decreased significantly. Preoperative IS/OS junction defect and ELM defect were both related to sensitive （r=-0.55, -0.53; P＜0.05）, but uncorrelated with BCVA （r=0.13, 0.13; P＞0.05）. IS/OS junction defect and ELM defect 1st, 3rd and 6th months after surgery were both related to MS and BCVA （P＜0.05）. Conclusions The logMAR BCVA and MS increases, while IS/OS junction and defect ELM defect decreases after surgery in IMH patients. IS/OS junction defect and ELM defect after surgery were both related to sensitive and BCVA.
ObjectiveTo observe the protective effect of human umbilical cord blood stem cells (hUCBSC) transplantation on retinal ganglion cells (RGC) after optic nerve injury. Method48 adult Sprague-Dawley rats were randomly divided into group A and B, therefore 24 rats in each group. Calibrated optic nerve crush injury model was induced in the left eyes, the right eyes served as a control. Medicine was injected at seventh day after optic nerve injury. PBS was injected into the eyes of Group A rats by peribulbar injection. The hUCBSCs were injected into the eyes of Group B rats by peribulbar injection. Seven days before sacrifice, 5% fluorogold was injected into superior colliculi bilaterally. At 7, 14, 21, 28 days after labeled, retinal flat mounts were observed under fluorescence microscope and optical microscope to investigate the morphological and RGC changes in density during retinal degeneration. ResultsThe RGC number showed a tendency to decline gradually along with increases of the time in two groups, but the trend of decrease of Group B was evidently slower than that of Group A. The RGC number of the injury eye were less than the control eye in Group A and B (t=3.24, 3.15; P < 0.05). At 7, 14, 21, 28 days after labeled, the RGC number (t=4.78, 4.70, 3.98, 3.27; P < 0.05) and labeled RGC rate (t=4.39, 4.21, 4.36, 5.07; P < 0.05) in group B were more than those in group A. After optic nerve injury, there was karyopycnosis on ganglion cell layer of retina, thinning on each layer of retina, derangement of cell and decrease in RGC. There was different degree of the above change in different time after optic nerve injury. There were the swelling, the hemorrhage, derangement of spongiocyte and the denaturation like vacuole in the spot of optic nerve injury. Moreover, they were aggravating with increases of the time after optic nerve injury. There was no pathological changes in normal eyes. ConclusionThe hUCBSC can increase the survival rate of the RGC and can rescue and(or) restore the injujed RGC after transplanted into body of optic nerve crush rat model by peribulbar injection.