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Cited by 102Corneal Surgery and TreatmentsWound Healing and TreatmentsNF-κB Signaling Pathways

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Therapeutic Effect of Topical Administration of SN50, an Inhibitor of Nuclear Factor-κB, in Treatment of Corneal Alkali Burns in Mice

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Saika, Shizuya, Miyamoto, Takeshi, Yamanaka, Osamu, Kato, Tadashi, Ohnishi, Yoshitaka, Flanders, Kathleen C., Ikeda, Kazuo, Nakajima, Yuji, Kao, Winston W.-Y., Sato, Misako, Muragaki, Yasuteru, Ooshima, Akira·2005·The American Journal of Pathology
DOI 10.1016/s0002-9440(10)62357-7PMC PMC1606394
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Abstract

We evaluated the therapeutic efficacy of topical administration of SN50, an inhibitor of nuclear factor-kappaB, in a corneal alkali burn model in mice. An alkali burn was produced with 1 N NaOH in the cornea of C57BL/6 mice under general anesthesia. SN50 (10 microg/microl) or vehicle was topically administered daily for up to 12 days. The eyes were processed for histological or immunohistochemical examination after bromodeoxyuridine labeling or for semi-quantification of cytokine mRNA. Topical SN50 suppressed nuclear factor-kappaB activation in local cells and reduced the incidence of epithelial defects/ulceration in healing corneas. Myofibroblast generation, macrophage invasion, activity of matrix metalloproteinases, basement membrane destruction, and expression of cytokines were all decreased in treated corneas compared with controls. To elucidate the role of tumor necrosis factor (TNF)-alpha in epithelial cell proliferation, we performed organ culture of mouse eyes with TNF-alpha, SN50, or an inhibitor of c-Jun N-terminal kinase (JNK) and examined cell proliferation in healing corneal epithelium in TNF-alpha-/- mice treated with SN50. An acceleration of epithelial cell proliferation by SN50 treatment was found to depend on TNF-alpha/JNK signaling. In conclusion, topical application of SN50 is effective in treating corneal alkali burns in mice.

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  • Recent studies suggest a connection between TNF-α and NFκB activity in corneal wound healing after alkali injury.

    “In addition, recent studies suggest a connection between TNF-α and NFκB activity in corneal wound healing after alkali injury (Saika et al., 2005).”

    From Thymosin beta 4 suppression of corneal NFκB: A potential anti-inflammatory pathway (2007) · cites this paper as Saika et al., 2005

  • The use of TNF-α as a pro-inflammatory stimulus in the cell culture model has important physiological relevance to corneal inflammation and epithelial wound healing.

    “The use of TNF-α as a pro-inflammatory stimulus in our cell culture model has important physiological relevance to corneal inflammation and epithelial wound healing.”

    From Thymosin beta 4 suppression of corneal NFκB: A potential anti-inflammatory pathway (2007) · cites this paper as Saika et al., 2005

  • TNF-α is increased in tears during infections and inflammations of the cornea.

    “This is because TNF-α is increased in tears during infections and inflammations of the cornea, suggesting its importance as a mediator of inflammation in vitro as well as in vivo (Bitko et al., 2004; Kumar et al., 2004; Saika et al., 2005).”

    From Thymosin beta 4 suppression of corneal NFκB: A potential anti-inflammatory pathway (2007) · cites this paper as Saika et al., 2005

    The introduction discusses inflammation after corneal alkali burns, and the section on TNF-α/JNK signaling examines TNF-α in healing mouse corneal epithelium. Searches for TNF-α in tears and for corneal infection found no passage reporting that tear TNF-α increases during infections or inflammation. The cited paper therefore does not verify the specific claim about tears. (LLM, conf=0.76)

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Metadata

Authors
Saika, S., Miyamoto, T., Yamanaka, O., Kato, T., Ohnishi, Y., Flanders, K. C., Ikeda, K., Nakajima, Y., Kao, W. W.-Y., Sato, M., Muragaki, Y., & Ooshima, A.
Affiliations
  • Wakayama Medical University (JP)
  • National Institutes of Health (US)
  • Osaka City University (JP)
  • University of Cincinnati Medical Center (US)
Corresponding author
Saika, Shizuya
ORCID
Venue
The American Journal of Pathology
Publisher
Elsevier BV
Published
2005-05
Volume
166
Issue
5
Pages
1393-1403
ISSN
0002-9440 (ISSN-L)
DOI
10.1016/s0002-9440(10)62357-7
PMC
PMC1606394
OpenAlex
W2021447146
Cited by
102
References
2
Citations by year
2026: 2 · 2025: 2 · 2024: 1 · 2023: 5 · 2022: 1 · 2021: 5 · 2020: 5 · 2019: 1 · 2018: 6 · 2017: 8 · 2016: 4 · 2015: 9 · 2014: 3 · 2013: 4 · 2012: 6
FWCI
5.88
Type
journal article
Language
en
Open access
Licence
Locations
  • American Journal Of Pathology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Wakayama Medical University
  • Research to Prevent Blindness
  • Ohio Lions Eye Research Foundation
  • Uehara Memorial Foundation
  • National Institutes of Health (EY 13755)
  • Ministry of Education, Culture, Sports, Science and Technology
Topics
  • Health Sciences › Medicine › Ophthalmology › Corneal Surgery and Treatments
  • Health Sciences › Medicine › Surgery › Wound Healing and Treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
Keywords
SN50, NF-κB inhibitors, corneal alkali burn, topical administration, corneal epithelial wound healing, TNF-α, JNK signaling, corneal epithelial cell proliferation, macrophage infiltration, matrix metalloproteinases, corneal ulcer, keratitis
MeSH terms
Administration, Topical, Alkalies, Animals, Basement Membrane, Burns, Chemical, Cornea, Corneal Stroma, Eye Burns, Fibroblasts, Macrophages, Male, Mice, Inbred C57BL, Monocytes, Peptides, Tumor Necrosis Factor-alpha, Wound Healing, Signal Transduction, Cytokines, NF-kappa B, Tissue Inhibitor of Metalloproteinase-1, Myocytes, Smooth Muscle, Metalloproteases, JNK Mitogen-Activated Protein Kinases, Mice, Corneal Injuries

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