Experimental evaluation of Folic acid effect on Corneal burn ulcer healing in new Zealand white rabbit

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Mahlojiyan AmirHossein; Jahandideh Alireza; ASGHARI AHMAD; mortezavi pezhman

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Journal: VETERINARY CLINICAL PATHOLOGY (VETERINARY JOURNAL TABRIZ) Year:2020 | Volume:13 | Issue:4 (52) Page(s): 371-383

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Title

Experimental evaluation of Folic acid effect on Corneal burn ulcer healing in new Zealand white rabbit

Author(s)

Mahlojiyan AmirHossein | Jahandideh Alireza | ASGHARI AHMAD | mortezavi pezhman | Issue Writer Certificate

Keywords

Folic acidQ1

Corneal ulcersQ2

RabbitQ2

antioxidantsQ2

Abstract

Background and Purpose: Corneal ulcer is one of the most common eye diseases, which can be caused by trauma, chemical agents, and some bacteria, viruses, and chlamydia. Treatment of corneal ulcer has been always a concern in ophthalmology. This concern is due to the major role of cornea in providing and preserving normal vision. Alkali-induced corneal ulcer creates an intense inflammatory reaction to traumatic injuries and this intense inflammation can inhibit the natural epithelial growth and cause fibrosis or scar on cornea. Cornea is an organ in the eye that creates a smooth and clear surface and so, it provides the possibility of light regularly passing through the eye. Any injury of this layer eliminates its transparency and protective capacity. Cornea has few cells and no vessels. Various bacterial, viral, parasitic, and fungal agents can cause severe infections in cornea. After the occurrence of corneal injury, the cells surrounding the injured area including epithelial, stromal, and endothelial cells try to improve the injury by cell division and calling the immune system cells such as neutrophils, macrophages, and monocytes; as a result of this process, the injured area becomes inflamed and edematous. In most cases, due to basic membrane decay and leakage of proteinase, epithelial cells will not be able to provide the connections required for retrieving the layers. So, the distance between epithelial cells increase and the bond between them become weak. As a result of corneal ulcer, increased activity of destructive proteinases and decreased activity of proteases leads to rapid detachment of collagen and other extracellular components of corneal matrix. Significant increase of reactive oxygen species (ROS), increased oxidative condition, and decreased components of antioxidant system occur following corneal injury. In histological studies, various cells of immune system including neutrophils, lymphocytes, monocytes, and macrophages are found in cornea. Increased reactive oxygen species (ROS), increased oxidative stress, and decreased components of antioxidant system are observed in pathologic conditions and in the case of corneal injury. Various studies have reported the role of antioxidants in prevention and treatment of corneal ulcer. The recent studies have indicated that Folic acid restores decreased enzymatic and non-enzymatic antioxidants. also, its improving effect is due to inhibition of reactive oxygen species (ROS).

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APA: Copy

Mahlojiyan, AmirHossein, Jahandideh, Alireza, ASGHARI, AHMAD, & mortezavi, pezhman. (2020). Experimental evaluation of Folic acid effect on Corneal burn ulcer healing in new Zealand white rabbit. VETERINARY CLINICAL PATHOLOGY (VETERINARY JOURNAL TABRIZ), 13(4 (52) ), 371-383. SID. https://sid.ir/paper/183030/en

Vancouver: Copy

Mahlojiyan AmirHossein, Jahandideh Alireza, ASGHARI AHMAD, mortezavi pezhman. Experimental evaluation of Folic acid effect on Corneal burn ulcer healing in new Zealand white rabbit. VETERINARY CLINICAL PATHOLOGY (VETERINARY JOURNAL TABRIZ)[Internet]. 2020;13(4 (52) ):371-383. Available from: https://sid.ir/paper/183030/en

IEEE: Copy

AmirHossein Mahlojiyan, Alireza Jahandideh, AHMAD ASGHARI, and pezhman mortezavi, “Experimental evaluation of Folic acid effect on Corneal burn ulcer healing in new Zealand white rabbit,” VETERINARY CLINICAL PATHOLOGY (VETERINARY JOURNAL TABRIZ), vol. 13, no. 4 (52) , pp. 371–383, 2020, [Online]. Available: https://sid.ir/paper/183030/en

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