Dergiler / Glokom Katarakt / 2021 / Cilt: 16 - Sayı: 3

Can Endoplasmic Reticulum Stress Inhibition Reduce Inflammation Due to Alkaline Corneal Burns? -Preliminary Report-

Sayfa
167–170
Yayın Tarihi
2022-10-18
DOI
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⚡ TL;DR(1 Cümlede Hızlı Çıkarım)

More comprehensive and comparative studies should be conducted on this subject.

📌 3 Maddede Bu Makale

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Amaç & Hipotez:Purpose: The role of endoplasmic reticulum stress has not yet been investigated in corneal inflammation.
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Temel Bulgular & Veri:The study was carried out on Wistar rats of 250- 300 mg divided into four groups, with 1 animal in each group.
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Sonuç & Katkı:More comprehensive and comparative studies should be conducted on this subject.
🔬Tür:Modelleme & Sayısal Simülasyon
📍Kapsam:Genişletilmiş Akademik Örneklem
⚙️Değişkenler:Alan Parametreleri

Abstract

Purpose: The role of endoplasmic reticulum stress has not yet been investigated in corneal inflammation. In this preliminary study, we aimed to find out whether endoplasmic reticulum stress inhibition has an effect on inflammation and neovascularization after alkaline burn and to find the effective dose. Materials and Methods: Salubrinal was used as an endoplasmic reticulum stress inhibitor. The study was carried out on Wistar rats of 250- 300 mg divided into four groups, with 1 animal in each group. After the corneal neovascularization (CNV) model was created in the right eyes, subconjunctival salubrinal was administered at doses of 0.1; 0.25; 0.5 and 1 mg/kg respectively. Subconjunctival Salubrinal was applied to the left eyes without creating a CNV model. Histopathological results were evaluated in the corneal tissues taken from animals that were sacrificed on the 14th day. Results: As a result of histopathological evaluation performed in 4 groups, inflammation and vascularization were observed in the groups given 0.1 mg / kg, 0.25 mg / kg and 0.5 mg / kg salubrinal, respectively. In the group given 1 mg / kg salurinal, it was observed that inflammation was less than the other groups and there was no vascular structures. In any group, salubrinal did not show toxic effects on intact corneal tissue histologically. Discussion: Inhibition of endoplasmic reticulum stress, which is a pathway of inflammation, can be used in the treatment of inflammation and corneal neovascularization caused by alkaline burns. More comprehensive and comparative studies should be conducted on this subject.

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Bu Makaleye Atıf Yap

CANKARA, F. N., SAVRAN, M., ASCI, H., GÜLLE, K., KARACA, U., USTA, G. (2022). Can Endoplasmic Reticulum Stress Inhibition Reduce Inflammation Due to Alkaline Corneal Burns? -Preliminary Report-. Glokom Katarakt, Cilt: 16 - Sayı: 3, 167–170. https://ajindex.com/articles/525728

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Kaynakça (16)

  1. Zhang K, Kaufman RJ. From endoplasmic-reticulum stress to the inflammatory response. Nature 2008;454:455-62
  2. Zhang B, Li M, Zou Y, et al. NFκB/Orai1 Facilitates Endoplasmic Reticulum Stress by Oxidative Stress in the Pathogenesis of Non- alcoholic Fatty Liver Disease. Front Cell Dev Biol 2019;7:202
  3. Cao SS, Luo KL, Shi L. Endoplasmic Reticulum Stress Interacts With Inflammation in Human Diseases. J Cell Physiol 2016;231:288-94
  4. Zhang L, Xia Q, Zhou Y, et al. Endoplasmic reticulum stress and autophagy contribute to cadmium-induced cytotoxicity in retinal pigment epithelial cells. Toxicol Lett 2019;311:105-113
  5. Boyce M, Bryant KF, Jousse C, et al. A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress. Science 2005;307:935-9
  6. Matsuoka M, Komoike Y. Experimental Evidence Shows Salubrinal, an eIF2α Dephosphorylation Inhibitor, Reduces Xenotoxicant-Induced Cellular Damage. Int J Mol Sci 2015;16:16275-87
  7. Mahoney JM, Waterbury LD. Drug effects on the neovascularization response to silver nitrate cauterization of the rat cornea. Curr Eye Res 1985;4:531-5
  8. Hu Y, Lu X, Xu Y, et al. Salubrinal attenuated retinal neovascularization by inhibiting CHOP-HIF1α-VEGF pathways. Oncotarget 2017;8:77219-32
  9. Wek RC, Cavener DR. Translational control and the unfolded protein response. Antioxid Redox Signal 2007;9:2357-71
  10. Boyce M, Yuan J. Cellular response to endoplasmic reticulum stress: a matter of life or death. Cell Death Differ 2006;13:363- 73
  11. Abdelfattah NS, Amgad M, Zayed AA, et al. Molecular underpinnings of corneal angiogenesis: advances over the past decade. Int J Ophthalmol 2016;9:768-79
  12. Cursiefen C, Chen L, Borges LP, et al. VEGF-A stimulates lymphangiogenesis and hemangiogenesis in inflammatory neovascularization via macrophage recruitment. J Clin Invest 2004;113:1040-50
  13. Roshandel D, Eslani M, Baradaran-Rafii A, et al. Current and emerging therapies for corneal neovascularization. Ocul Surf 2018;16:398-414
  14. Li J, Cai X, Xia Q, et al. Involvement of endoplasmic reticulum stress in all-trans-retinal-induced retinal pigment epithelium degeneration. Toxicol Sci 2015;143:196-208
  15. Wang Y, Osakue D, Yang E, et al. Endoplasmic Reticulum Stress Response of Trabecular Meshwork Stem Cells and Trabecular Meshwork Cells and Protective Effects of Activated PERK Pathway. Invest Ophthalmol Vis Sci 2019;60:265-273
  16. Yao J, Bi HE, Sheng Y, et al. Ultraviolet (UV) and hydrogen peroxide activate ceram