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目的：观察己酮可可碱（ＰＴＸ）对创伤性急性肺损伤（ＡＬＩ）家兔肺组织肿瘤坏死因子 α基因（ＴＮＦ αｍ ＲＮＡ）表达的影响，探讨ＰＴＸ在创伤性ＡＬＩ治疗中的作用机制。方法：采用创伤性ＡＬＩ模型，实验动物随机分为正常对照组（８ 只）、创伤性ＡＬＩ模型组（２４ 只）和ＰＴＸ治疗组（２４ 只），用ＥＬＩＳＡ 和逆转录聚合酶链反应（ＲＴ ＰＣＲ）方法分别检测不同时间点血浆ＴＮＦ α含量及肺组织ＴＮＦ αｍ ＲＮＡ表达水平。结果：血浆ＴＮＦ α含量创伤性ＡＬＩ模型组于创伤后１．５ 小时达峰值〔（１．２７±０．２６）μｇ／Ｌ〕，肺组织ＴＮＦ αｍ ＲＮＡ表达于创伤后８ 小时达高峰（２．６７±０．１８），二者在时间上不完全平行。ＰＴＸ治疗组肺组织ＴＮＦ αｍ ＲＮＡ 的表达和外周血ＴＮＦ α含量均低于创伤性ＡＬＩ模型组（Ｐ均＜ ０．０５）。结论：ＰＴＸ能有效抑制创伤性ＡＬＩ家兔肺组织ＴＮＦ αｍ ＲＮＡ表达；本研究为ＰＴＸ治疗创伤性ＡＬＩ提供了实验依据。
Objective: To investigate the effect of pentoxifylline (PTX) on the expression of tumor necrosis factor α (TNFαmRNA) in lung tissue of rabbits with traumatic acute lung injury (ALI) and explore the mechanism of PTX in the treatment of traumatic ALI. Methods: The traumatic ALI model was used in this study. The experimental animals were randomly divided into normal control group (n = 8), traumatic ALI model group (n = 24) and PTX treatment group (n = 24). ELISA and reverse transcription polymerase chain reaction PCR) were used to detect the levels of plasma TNFα and TNFαmRNA in lung tissue at different time points. Results: The plasma level of TNFα in traumatic ALI model reached its peak at 1.5 hour after trauma (1.27 ± 0.26) μg / L〕. The expression of TNFαmRNA in lung tissue peaked at 8 hours after trauma (2 .67 ± 0.18), both of which are not completely parallel in time. The expression of TNFαmRNA and the level of TNFα in peripheral blood of PTX treatment group were lower than that of traumatic ALI model group (all P <0.05). CONCLUSION: PTX can effectively inhibit the expression of TNFαmRNA in the lung tissue of traumatic ALI rabbits. This study provides an experimental basis for the treatment of traumatic ALI by PTX.