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Updated: Jun 22, 2026
Recurrent Herpetic Stromal Keratitis in Mice, a Model for Studying Human HSK
Published on: December 18, 2012
Lornoxicam suppresses recurrent herpetic stromal keratitis through down-regulation of nuclear factor-kappaB: an
Jie Yin1, Zhenping Huang, Yuan Xia
1Department of Ophthalmology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, People's Republic of China.
Purpose:
We designed the current study to determine the protective effects of lornoxicam, a cyclooxygenase (COX) inhibitor, on recurrent herpetic stromal keratitis (HSK) and the nuclear factor-kappaB (NF-kappaB)-mediated mechanism in mice.
Methods:
A corneal latent herpes simplex virus-1 (HSV-1) infected mouse model was established. Six weeks later, Ultraviolet B (UVB) irradiation induced the recurrence. Corneal swabs were obtained and cultured with indicator cells to determine shedding of the virus. Lornoxicam was administered intraperitoneally daily, beginning one day before irradiation and lasting for seven days. Saline-treated and mock-infected control groups were also studied at the same time. Development of corneal inflammation and opacity was scored. Immunohistochemical staining and an electrophoretic mobility shift assay were performed to evaluate the effect of lornoxicam on NF-kappaB activation in the corneal tissues. The levels of tumor necrosis factor-alpha (TNF-alpha) in the cornea were determined by an enzyme-linked immunosorbent assay (ELISA).
Results:
HSV-1 reactivation induced stromal edema and opacification concomitantly with elevated activation of NF-kappaB and elevated production of TNF-alpha. Lornoxicam treatment significantly decreased the incidence of recurrent HSK, attenuated the corneal opacity scores, and also effectively suppressed both NF-kappaB activation and TNF-alpha expression in biological analysis. Histopathology examination revealed a reduced immunostaining positive cell density for NF-kappaB in the cornea from lornoxicam-treated mice as well as a diminished inflammatory response.
Conclusions:
Lornoxicam exerts protective effects against HSK, presumably through the down-regulation of NF-kappaB activation.
Insights
Lornoxicam, a cyclooxygenase (COX) inhibitor, effectively reduced recurrent herpetic stromal keratitis (HSK) in mice. This protection is linked to the down-regulation of nuclear factor-kappaB (NF-kappaB) activation and associated inflammatory responses.
Area of Science:
- Ophthalmology
- Immunology
- Pharmacology
Background:
- Herpetic stromal keratitis (HSK) is a significant cause of vision loss.
- Recurrence of HSK is often triggered by factors like ultraviolet B (UVB) irradiation.
- The nuclear factor-kappaB (NF-kappaB) pathway is implicated in the inflammatory mechanisms of HSK.
Purpose of the Study:
- To investigate the protective effects of lornoxicam, a cyclooxygenase (COX) inhibitor, against recurrent HSK in a mouse model.
- To elucidate the role of the nuclear factor-kappaB (NF-kappaB) pathway in lornoxicam's protective mechanism against HSK.
Main Methods:
- A mouse model of latent herpes simplex virus-1 (HSV-1) corneal infection was established and reactivated using UVB irradiation.
- Lornoxicam was administered intraperitoneally to assess its impact on viral shedding, corneal inflammation, and opacity.
- NF-kappaB activation, tumor necrosis factor-alpha (TNF-alpha) levels, and inflammatory responses were evaluated using immunohistochemistry, electrophoretic mobility shift assay, and ELISA.
Main Results:
- Recurrent HSK was characterized by stromal edema, opacity, elevated NF-kappaB activation, and increased TNF-alpha production.
- Lornoxicam treatment significantly reduced the incidence of recurrent HSK and attenuated corneal opacity.
- Lornoxicam effectively suppressed NF-kappaB activation and TNF-alpha expression, leading to a diminished inflammatory response in the cornea.
Conclusions:
- Lornoxicam demonstrates significant protective effects against recurrent herpetic stromal keratitis in mice.
- The protective mechanism of lornoxicam is likely mediated through the down-regulation of NF-kappaB activation.
