Protective effect of etanercept, an inhibitor of tumor necrosis factor-α, in a rat model of retinal ischemia

Hyoung Won Bae, Naeun Lee, Gong Je Seong, Seungsoo Rho, Samin Hong, Chan Yun Kim

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Background: To assess the neuroprotective effect of etanercept (Enbrel®) which is a commercialized Tumor necrosis factor-α (TNF-α) inhibitor on axonal injury in an animal model of acute ischemia. Methods: Acute ischemia was induced by intraocular pressure elevation in 36 rats. The treatment groups underwent subcutaneous injection of etanercept (0.3 or 1.0 mg/kg) three times per week up to 4 weeks. The control groups were treated in the same manner using the same volume of phosphate-buffered saline (PBS). Optic nerve damage was evaluated by counting the number of axons under a transmission electron microscope. Microglial cell activity was assessed using Iba1 and CD68. Results: After induction of ischemia, the ratio of preserved axons was significantly greater in the 2-week 1.0-mg/kg etanercept-treated group than in the PBS-treated group (p = 0.062). The 4-week 0.3-mg/kg and 1.0-mg/kg etanercept-treated groups also showed significantly higher ratios of preserved axons than did the PBS-treated group (p = 0.021 and 0.003, respectively). The expression of Iba1 and CD68 in the optic nerve was lower in the etanercept-treated groups than in the PBS-treated groups. Immunohistochemical staining using rabbit anti-Iba1 antibody showed that the amount of microglia at the optic nerve head was noticeably lower in the etanercept-treated groups than in the PBS-treated groups. Conclusions: Etanercept significantly suppressed optic nerve injury in this rat model of acute ischemia. This in vivo study suggests that etanercept might be a novel neuroprotective treatment agent for TNF-α-related disease.

Original languageEnglish
Article number16
JournalBMC Ophthalmology
Volume16
Issue number1
DOIs
Publication statusPublished - 2016 Jun 4

Fingerprint

Ischemia
Tumor Necrosis Factor-alpha
Phosphates
Axons
Neuroprotective Agents
Optic Nerve
Optic Nerve Injuries
Etanercept
Optic Disk
Microglia
Subcutaneous Injections
Intraocular Pressure
Anti-Idiotypic Antibodies
Animal Models
Electrons
Staining and Labeling
Rabbits
Control Groups
Wounds and Injuries
Therapeutics

All Science Journal Classification (ASJC) codes

  • Ophthalmology

Cite this

Bae, Hyoung Won ; Lee, Naeun ; Seong, Gong Je ; Rho, Seungsoo ; Hong, Samin ; Kim, Chan Yun. / Protective effect of etanercept, an inhibitor of tumor necrosis factor-α, in a rat model of retinal ischemia. In: BMC Ophthalmology. 2016 ; Vol. 16, No. 1.
@article{0b8c0d5d89b04f03b1db7204098652e4,
title = "Protective effect of etanercept, an inhibitor of tumor necrosis factor-α, in a rat model of retinal ischemia",
abstract = "Background: To assess the neuroprotective effect of etanercept (Enbrel{\circledR}) which is a commercialized Tumor necrosis factor-α (TNF-α) inhibitor on axonal injury in an animal model of acute ischemia. Methods: Acute ischemia was induced by intraocular pressure elevation in 36 rats. The treatment groups underwent subcutaneous injection of etanercept (0.3 or 1.0 mg/kg) three times per week up to 4 weeks. The control groups were treated in the same manner using the same volume of phosphate-buffered saline (PBS). Optic nerve damage was evaluated by counting the number of axons under a transmission electron microscope. Microglial cell activity was assessed using Iba1 and CD68. Results: After induction of ischemia, the ratio of preserved axons was significantly greater in the 2-week 1.0-mg/kg etanercept-treated group than in the PBS-treated group (p = 0.062). The 4-week 0.3-mg/kg and 1.0-mg/kg etanercept-treated groups also showed significantly higher ratios of preserved axons than did the PBS-treated group (p = 0.021 and 0.003, respectively). The expression of Iba1 and CD68 in the optic nerve was lower in the etanercept-treated groups than in the PBS-treated groups. Immunohistochemical staining using rabbit anti-Iba1 antibody showed that the amount of microglia at the optic nerve head was noticeably lower in the etanercept-treated groups than in the PBS-treated groups. Conclusions: Etanercept significantly suppressed optic nerve injury in this rat model of acute ischemia. This in vivo study suggests that etanercept might be a novel neuroprotective treatment agent for TNF-α-related disease.",
author = "Bae, {Hyoung Won} and Naeun Lee and Seong, {Gong Je} and Seungsoo Rho and Samin Hong and Kim, {Chan Yun}",
year = "2016",
month = "6",
day = "4",
doi = "10.1186/s12886-016-0262-9",
language = "English",
volume = "16",
journal = "BMC Ophthalmology",
issn = "1471-2415",
publisher = "BioMed Central",
number = "1",

}

Protective effect of etanercept, an inhibitor of tumor necrosis factor-α, in a rat model of retinal ischemia. / Bae, Hyoung Won; Lee, Naeun; Seong, Gong Je; Rho, Seungsoo; Hong, Samin; Kim, Chan Yun.

In: BMC Ophthalmology, Vol. 16, No. 1, 16, 04.06.2016.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Protective effect of etanercept, an inhibitor of tumor necrosis factor-α, in a rat model of retinal ischemia

AU - Bae, Hyoung Won

AU - Lee, Naeun

AU - Seong, Gong Je

AU - Rho, Seungsoo

AU - Hong, Samin

AU - Kim, Chan Yun

PY - 2016/6/4

Y1 - 2016/6/4

N2 - Background: To assess the neuroprotective effect of etanercept (Enbrel®) which is a commercialized Tumor necrosis factor-α (TNF-α) inhibitor on axonal injury in an animal model of acute ischemia. Methods: Acute ischemia was induced by intraocular pressure elevation in 36 rats. The treatment groups underwent subcutaneous injection of etanercept (0.3 or 1.0 mg/kg) three times per week up to 4 weeks. The control groups were treated in the same manner using the same volume of phosphate-buffered saline (PBS). Optic nerve damage was evaluated by counting the number of axons under a transmission electron microscope. Microglial cell activity was assessed using Iba1 and CD68. Results: After induction of ischemia, the ratio of preserved axons was significantly greater in the 2-week 1.0-mg/kg etanercept-treated group than in the PBS-treated group (p = 0.062). The 4-week 0.3-mg/kg and 1.0-mg/kg etanercept-treated groups also showed significantly higher ratios of preserved axons than did the PBS-treated group (p = 0.021 and 0.003, respectively). The expression of Iba1 and CD68 in the optic nerve was lower in the etanercept-treated groups than in the PBS-treated groups. Immunohistochemical staining using rabbit anti-Iba1 antibody showed that the amount of microglia at the optic nerve head was noticeably lower in the etanercept-treated groups than in the PBS-treated groups. Conclusions: Etanercept significantly suppressed optic nerve injury in this rat model of acute ischemia. This in vivo study suggests that etanercept might be a novel neuroprotective treatment agent for TNF-α-related disease.

AB - Background: To assess the neuroprotective effect of etanercept (Enbrel®) which is a commercialized Tumor necrosis factor-α (TNF-α) inhibitor on axonal injury in an animal model of acute ischemia. Methods: Acute ischemia was induced by intraocular pressure elevation in 36 rats. The treatment groups underwent subcutaneous injection of etanercept (0.3 or 1.0 mg/kg) three times per week up to 4 weeks. The control groups were treated in the same manner using the same volume of phosphate-buffered saline (PBS). Optic nerve damage was evaluated by counting the number of axons under a transmission electron microscope. Microglial cell activity was assessed using Iba1 and CD68. Results: After induction of ischemia, the ratio of preserved axons was significantly greater in the 2-week 1.0-mg/kg etanercept-treated group than in the PBS-treated group (p = 0.062). The 4-week 0.3-mg/kg and 1.0-mg/kg etanercept-treated groups also showed significantly higher ratios of preserved axons than did the PBS-treated group (p = 0.021 and 0.003, respectively). The expression of Iba1 and CD68 in the optic nerve was lower in the etanercept-treated groups than in the PBS-treated groups. Immunohistochemical staining using rabbit anti-Iba1 antibody showed that the amount of microglia at the optic nerve head was noticeably lower in the etanercept-treated groups than in the PBS-treated groups. Conclusions: Etanercept significantly suppressed optic nerve injury in this rat model of acute ischemia. This in vivo study suggests that etanercept might be a novel neuroprotective treatment agent for TNF-α-related disease.

UR - http://www.scopus.com/inward/record.url?scp=84971613854&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84971613854&partnerID=8YFLogxK

U2 - 10.1186/s12886-016-0262-9

DO - 10.1186/s12886-016-0262-9

M3 - Article

C2 - 27259948

AN - SCOPUS:84971613854

VL - 16

JO - BMC Ophthalmology

JF - BMC Ophthalmology

SN - 1471-2415

IS - 1

M1 - 16

ER -