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Introduction: Retinal ischemia-reperfusion (IR) injury is associated with many ocular diseases. Retinal IR injury leads to the death of retinal ganglion cells (RGCs), loss of retinal function and ultimately vision loss. The aim of this study was to show the protective effects of prophylactic ozone administration against retinal IR injury.
Materials And Methods: A sham group (S) (n = 7) was administered physiological saline (PS) intraperitoneally (i.p.) for 7 d. An ischemia reperfusion (IR) group (n = 7) was subjected to retinal ischemia followed by reperfusion for 2 h. An ozone group (O) (n = 7) was administered 1 mg/kg of ozone i.p. for 7 d. In the ozone + IR (O + IR) group (n = 7), 1 mg/kg of ozone was administered i.p. for 7 d before the IR procedure and at 8 d, the IR injury was created (as in IR group). The rats were anesthetized after second hour of reperfusion and their intracardiac blood was drawn completely and they were sacrificed. Blood samples were sent to a laboratory for analysis of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), malondialdehyde (MDA), total oxidant score (TOS) and total antioxidant capacity (TAC). The degree of retinal injury was evaluated according to changes in retinal cells and necrotic and apoptotic cells using the TUNEL method. Data were evaluated statistically with the Kruskal-Wallis test.
Results: The number of RGCs and the inner retinal thickness were significantly decreased after ischemia, and treatment with ozone significantly inhibited retinal ischemic injury. In the IR group, the degree of retinal injury was found to be the highest. In the O + IR group, retinal injury was found to be decreased in comparison to the IR group. In the ozone group without retinal IR injury, the retinal injury score was the lowest. The differences in the antioxidant parameters SOD, GSH-Px and TAC were increased in the ozone group and the lowest in the IR group. The oxidant parameters MDA and TOS were found to be the highest in the IR group and decreased in the ozone group.
Discussion: IR injury is also positively correlated with the degree of early apoptosis. This study demonstrated that ozone can attenuate subsequent ischemic damage in the rat retina through triggering the increase of the antioxidant capacity.
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http://dx.doi.org/10.3109/15569527.2016.1156120 | DOI Listing |
J Vitreoretin Dis
September 2025
iMIND Study Group, Department of Ophthalmology, Duke University School of Medicine, Durham, NC, USA.
To assess retinal layer thickness and volume by optical coherence tomography (OCT) in patients with prior traumatic brain injury (TBI). Adults (≥18 years) with prior TBI were prospectively recruited. 512 × 128-mm macular cube scans were obtained using Zeiss Cirrus HD-5000 OCT.
View Article and Find Full Text PDFApoptosis
September 2025
Key Laboratory of Emergency and Trauma of the Ministry of Education, Department of Interventional Radiology and Vascular Surgery, First Affiliated Hospital of Hainan Medical University, Hainan Medical University, 31 Longhua Road, Longhua District, Haikou City, Hainan Province, China.
The singular forms of programmed cell death (PCD), including pyroptosis, apoptosis, and necroptosis, are inadequate for comprehensively elucidating the complex pathological mechanisms underlying ischemic diseases. PANoptosis is a unique lytic, innate immune, and inflammatory cell death pathway, initiated by innate immune sensors and driven by caspases and RIPKs through PANoptosome complexes. In diseases like cerebral ischemia, retinal ischemia, myocardial ischemia, renal ischemia, and spinal cord ischemia, targeting key regulatory factors of PANoptosis can help mitigate tissue damage.
View Article and Find Full Text PDFKidney360
September 2025
Division of Nephrology-Hypertension, Department of Medicine, University of California San Diego, San Diego California.
Background: CKD is strongly associated with cardiovascular disease (CVD), yet the etiology responsible for this link remains elusive. Novel blood and urine biomarkers reflecting kidney tubule dysfunction and injury may provide novel insights to mechanisms linking the kidney to CVD.
Methods: In 470 participants of the Multi-Ethnic Study of Atherosclerosis (MESA) without type 2 diabetes, CVD or CKD, we measured six plasma (kidney injury molecule-1 [KIM-1], monocyte chemoattractant protein-1 [MCP-1], soluble urokinase plasminogen activator receptor [suPAR], tumor necrosis factor receptor [TNFR] 1 and 2, and anti-chitinase-3-like protein 1 [YKL-40]) and six urinary (alpha 1 microglobulin [A-1M], epidermal growth factor [EGF], KIM-1, MCP-1, YKL-40 and uromodulin [UMOD]) kidney tubule health biomarkers.
Biology (Basel)
August 2025
Department of Oral Biology, The Dental College of Georgia, Augusta University, Augusta, GA 30912, USA.
The retina is highly sensitive to oxygen and blood supply, and hypoxia plays a key role in retinal diseases such as diabetic retinopathy (DR) and age-related macular degeneration (AMD). Müller glial cells, which are essential for retinal homeostasis, respond to injury and hypoxia with reactive gliosis, characterized by the upregulation of the glial fibrillary acidic protein (GFAP) and vimentin, cellular hypertrophy, and extracellular matrix changes, which can impair retinal function and repair. The retinal pigment epithelium (RPE) supports photoreceptors, forms part of the blood-retinal barrier, and protects against oxidative stress; its dysfunction contributes to retinal degenerative diseases such as AMD, retinitis pigmentosa (RP), and Stargardt disease (SD).
View Article and Find Full Text PDFNeural Regen Res
September 2025
Guangdong-Hongkong-Macau Institute of CNS Regeneration, Key Laboratory of CNS Regeneration (Ministry of Education), Guangdong Key Laboratory of Non-human Primate Research, Jinan University, Guangzhou, Guangdong Province, China.
Optic nerve injury leads to axonal degeneration and the death of retinal ganglion cells, which ultimately causes vision loss. Notably, current treatments are limited. In the present study, we explored whether neurogenic differentiation factor 1 (NeuroD1 or ND1) overexpression in retinal Müller cells may repair the retina after optic nerve crush in mice.
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