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目的探讨双氟灭病钠治疗角膜穿膜通伤的机理，并加以论证，为其临床应用提供基础理论依据。方法在兔眼建立角膜穿通伤模型，分别以生理盐水、0．1％地塞米松治疗，取伤后1d、3d、7d、14d房水检测IL－1TNFα。结果各时段两药物治疗组与对照组IL－1TNFα的活性和含量明显受到抑制。结论双氟灭痛钠治疗角膜穿通伤的机理在于有效地抑制了IL－1和TNFα的生物合成和释放。
Objective To investigate the mechanism of sodium fluoride in the treatment of corneal penetrating injury, and to be demonstrated, to provide the basic theoretical basis for its clinical application. Methods Corneal penetrating injury model was established in rabbit eyes. The rats were treated with normal saline and 0.1% dexamethasone respectively. IL-1 TNFα was detected in aqueous humor at 1, 3, 7 and 14 days after injury. Results The activity and content of IL-1TNFα in the two drug treatment groups and the control group were significantly inhibited at different time points. Conclusion The mechanism of PFD in treating corneal penetrating injury is to effectively inhibit the biosynthesis and release of IL-1 and TNFα.