Li Q, Luyo D, Matteson D M, Chan C C
Section on Immunopathology, National Eye Institute, National Institute of Health, Bethesda, MD, USA.
Ocul Immunol Inflamm. 1998 Jun;6(2):65-73. doi: 10.1076/ocii.6.2.65.4048.
Phospholipase A2s (PLA2s) are a family of esterases that initiate the arachidonic acid cascade, which results in the production of numerous inflammatory mediators. We investigated the expression of Group I and II PLA2 proteins and Group II mRNA in normal conjunctivae and in the conjunctivae of mice with compound 48/80-induced conjunctivitis. Conjunctivitis was induced in C57BL/6 mice by topical instillation of compound 48/80 (C48/80). Mice were then treated with corticosteroid (Pred Forte), antiflammin-2 (AF2, a synthetic peptide that inhibits PLA2), or a placebo (Dacriose, an isotonic, buffered, sterile eye irrigating solution). Low levels of PLA2s were detected on the epithelium of normal conjunctivae. One hr after C48/80 instillation, the expression of PLA2s appeared and increased in the substantia propria, peaked at 6 hr, and returned to baseline 72 hr later. Compared to the placebo, the conjunctivitis was moderate in the AF2-treated group and mild in Pred Forte-treated group. The expression of PLA2s was suppressed in mice treated with Pred Forte and AF2. iNOS mRNA was also diminished in the AF2- and Pred Forte-treated groups. The mechanisms by which anti-allergic medications suppress conjunctivitis may involve the inhibition of PLA2s and iNOS.
磷脂酶A2（PLA2）是一类酯酶，可启动花生四烯酸级联反应，从而产生多种炎症介质。我们研究了I组和II组PLA2蛋白以及II组mRNA在正常结膜和经化合物48/80诱导结膜炎的小鼠结膜中的表达情况。通过局部滴注化合物48/80（C48/80）在C57BL/6小鼠中诱导结膜炎。然后用皮质类固醇（强的松龙）、抗发炎蛋白-2（AF2，一种抑制PLA2的合成肽）或安慰剂（泪然，一种等渗、缓冲、无菌的眼部冲洗液）对小鼠进行治疗。在正常结膜上皮中检测到低水平的PLA2。滴注C48/80后1小时，PLA2在固有层中出现并增加，在6小时达到峰值，并在72小时后恢复到基线水平。与安慰剂相比，AF2治疗组的结膜炎为中度，强的松龙治疗组为轻度。在接受强的松龙和AF2治疗的小鼠中，PLA2的表达受到抑制。在AF2和强的松龙治疗组中，诱导型一氧化氮合酶（iNOS）mRNA也减少。抗过敏药物抑制结膜炎的机制可能涉及对PLA2和iNOS的抑制。
