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Keywords = intracameral oxygen

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9 pages, 1564 KB  
Article
Assessment of Efficacy of a Novel Crosslinking Protocol with Intracameral Oxygen (Bubble-CXL) in Increasing the Corneal Stiffness Using Atomic Force Microscopy
by Ammar Alkhalde, Hannah Seferovic, Ali Abri, Alvana Simbrunner, Peter Hinterdorfer and Yoo Jin Oh
Nanomaterials 2022, 12(18), 3185; https://doi.org/10.3390/nano12183185 - 14 Sep 2022
Cited by 4 | Viewed by 2415
Abstract
The environmental oxygen level plays a critical role in corneal crosslinking (CXL), a treatment method to increase corneal biomechanical stability. In this study, we introduce a new CXL method (Bubble-CXL), in which intracameral oxygen serves as an additional oxygen source during eye treatment. [...] Read more.
The environmental oxygen level plays a critical role in corneal crosslinking (CXL), a treatment method to increase corneal biomechanical stability. In this study, we introduce a new CXL method (Bubble-CXL), in which intracameral oxygen serves as an additional oxygen source during eye treatment. The efficiency of this new method was compared with the efficiency of the standard CXL method. Three fresh porcine eye pairs were included in this study. One eye of each pair was treated with standard CXL, whereas in the partner eye, intracameral oxygen was injected prior to CXL and removed at the end of the procedure. The Young’s modulus of each cornea was measured using atomic force microscopy. All analyzed corneas treated with intracameral oxygen showed significantly higher Young’s modulus and thus an increased stiffness compared to the cornea of the partner eye treated with the standard protocol. Using intracameral oxygen in CXL therapy may increase crosslinking efficiency and improve biomechanical corneal properties. Full article
(This article belongs to the Special Issue Cell and Matrix Biomechanics in Physiology and Pathology)
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17 pages, 9108 KB  
Article
Topical Ascorbic Acid Ameliorates Oxidative Stress-Induced Corneal Endothelial Damage via Suppression of Apoptosis and Autophagic Flux Blockage
by Yi-Jen Hsueh, Yaa-Jyuhn James Meir, Lung-Kun Yeh, Tze-Kai Wang, Chieh-Cheng Huang, Tsai-Te Lu, Chao-Min Cheng, Wei-Chi Wu and Hung-Chi Chen
Cells 2020, 9(4), 943; https://doi.org/10.3390/cells9040943 - 11 Apr 2020
Cited by 41 | Viewed by 5077
Abstract
Compromised pumping function of the corneal endothelium, due to loss of endothelial cells, results in corneal edema and subsequent visual problems. Clinically and experimentally, oxidative stress may cause corneal endothelial decompensation after phacoemulsification. Additionally, in vitro and animal studies have demonstrated the protective [...] Read more.
Compromised pumping function of the corneal endothelium, due to loss of endothelial cells, results in corneal edema and subsequent visual problems. Clinically and experimentally, oxidative stress may cause corneal endothelial decompensation after phacoemulsification. Additionally, in vitro and animal studies have demonstrated the protective effects of intraoperative infusion of ascorbic acid (AA). Here, we established a paraquat-induced cell damage model, in which paraquat induced reactive oxygen species (ROS) production and apoptosis in the B4G12 and ARPE-19 cell lines. We demonstrate that oxidative stress triggered autophagic flux blockage in corneal endothelial cells and that addition of AA ameliorated such oxidative damage. We also demonstrate the downregulation of Akt phosphorylation in response to oxidative stress. Pretreatment with ascorbic acid reduced the downregulation of Akt phosphorylation, while inhibition of the PI3K/Akt pathway attenuated the protective effects of AA. Further, we establish an in vivo rabbit model of corneal endothelial damage, in which an intracameral infusion of paraquat caused corneal opacity. Administration of AA via topical application increased its concentration in the corneal stroma and reduced oxidative stress in the corneal endothelium, thereby promoting corneal clarity. Our findings indicate a perioperative strategy of topical AA administration to prevent oxidative stress-induced damage, particularly for those with vulnerable corneal endothelia. Full article
(This article belongs to the Special Issue PI3K/AKT/mTOR Signaling Network in Human Health and Diseases)
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