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J. Yin, Z. Huang, Y. Xia, F. Ma, L. Wang, L. Zhang, H. Ma; Lornoxicam Suppresses Recurrent Herpetic Stromal Keratitis Through Down-Regulation of Nuclear Factor-B: Experimental Study in Mice. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4488.
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Cyclooxygenase (COX) inhibitors have been demonstrated to possess antiviral activity against ocular infection with Herpes simplex virus-1 (HSV-1). To determine the protective effects of lornoxicam, a cyclooxygenase (COX) inhibitor, on recurrent herpetic stromal keratitis (HSK) in mice and investigate whether this effect is via inhibition of nuclear factor-kappaB (NF-ΚB) activation.
ICR mice were infected with herpes simplex virus-1(HSV-1) strain McKrae (5µl of 106 Plaque Forming Units). After six weeks of latency, recurrence was induced by ultraviolet B irradiation. Corneal swabs were obtained and cultured with indicator cells to determine the shedding of virus. A COX inhibitor, lornoxicam, was administered intraperitoneally daily, beginning 1 day before irradiation and lasting for 7 days. Saline-treated group and mock infected control groups were studied at the same time. The development of corneal inflammation and opacity was recorded and scored. Immunohistochemical staining and an electrophoretic mobility shift assay were performed to evaluate the effect of lornoxicam on NF-ΚB activation in the cornea tissues. The levels of tumour necrosis factors-α (TNF-α) in the cornea were determined by enzyme-linked immunosorbent assay (ELISA).
HSV-1 reactivation induced stromal edema and opacification concomitantly with elevated activation of NF-ΚB and production of TNF-α. Lornoxicam treatment significantly decreased the incidence of recurrent HSK and attenuated the corneal opacity scores. Furthermore, lornoxicam effectively suppressed both NF-ΚB activation and TNF-α expression at each indicated time point (P<0.05). This is associated with a diminished inflammatory response and reduced immunostaining positive cell density for NF-ΚB in the corneas from lornoxicam-treated mice.
Lornoxicam exerts protective effect on recurrent HSK and may act through the down-regulation of NF-ΚB activation.
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