Abstract

To investigate the expression of interleukin-10 (IL-10) and the effect of NS-398(COX-2 inhibitor) on the expression of IL-10 in fungal keratitis in rats, and analyze its effects on anti-fungus immunity. Ninety Wister rats were randomly divided into 3 groups. Group A was blank control group (10 eyes). Group B was fungal keratitis group (40 eyes). Group C was fungal keratitis group treated with NS-398 (40 eyes). PAS staining, 100g/L potassium hydroxide (KOH) smear and fungal culture confirmed the successful establishment of fungal keratitis model. After the central epithelium was scraped, Fusarium solani colonies were applied and contact lens was put on the right cornea of group B and C, and plane contact lens was put on the left cornea of control eyes. Phosphate buffered saline (PBS) eyedrops were given for group B and NS-398 eyedrops for group C. The expression of IL-10 on corneas of group B and C on the 1(st) day, 3(rd) days, 7(th) days, and 14(th) days were detected by immunohistochemistry and semi- quantitative reverse transcription- polymerase chain reaction (RT-PCR). Histopathologic examination showed neutrophil infiltration and severe tissue necrosis in ulcer cornea. PAS staining confirmed the existence of hyphae and spores in the superficial layer of stroma. In the blank and control groups almost no expression of IL-10 was detected at any observing points. In group B the expression of IL-10 increased at first and decreased thereafter. Its expression also showed significant difference at any observing points (P<0.01). Compared with group B, the expression of IL-10 in group C showed no difference on the 1(st) day, decrease on the 3(rd) day, but a significant increase on the 7(th) day and 14(th) day. IL-10 takes part in the occurrence and development of fungal keratitis. NS-398 can upgrade the expression of IL-10 in fungal keratitis in the later period of the ulcer. Meanwhile, pathologic observation showed a slightly corneal opacity. IL-10 may play an important role in the process of cornea anti-damage repair.

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