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目的：ＴＮＦα参与伤口愈合的生物学调节的多个环节，本实验以老年大鼠为模型，观察阿霉素导致的慢性伤口愈合过程中血浆、组织ＴＮＦα的变化。方法：２４月龄大鼠在实验前４ｄ尾静脉注射阿霉素８ｍｇ／ｋｇ体重，然后背部切除直径为１５ｃｍ的皮肤，观察伤口区和血浆中ＴＮＦα在伤口愈合过程中的变化。结果：阿霉素可导致伤口愈合强度由对照组的（８６８±１５６）ｋｇ／ｃｍ２降至（６３６±１３６）ｋｇ／ｃｍ２（Ｐ＜００５），表现为伤口愈合障碍。阿霉素攻击后血液白细胞在第７ｄ降至最低，第１２ｄ回升至最高。此时阿霉素攻击第７ｄ血浆ＴＮＦα由实验前的（０７１±０６８）ｎｇ／Ｌ降至（０６５±０１０）ｎｇ／Ｌ，第１１ｄ为（０６８±０１５）ｎｇ／Ｌ，与实验前相比Ｐ＜００５。而生理盐水对照组则由实验前的（０７４±０１０）ｎｇ／Ｌ升至第１１ｄ（０８５±０１２）ｎｇ／Ｌ（Ｐ＜００５），与白细胞的变化趋势相近。阿霉素攻击后组织ＴＮＦα在第７ｄ为（４６２±１８６）ｎｇ／ｇ，与对照组（９９５±２．１６）ｎｇ／ｇ相比Ｐ＜００５，实验第１１ｄ两组ＴＮＦα都有升高，尤其阿霉素组升高至（１０６±１１２）ｎｇ／ｇ，比实?
OBJECTIVE: TNFα is involved in many aspects of the biological regulation of wound healing. In this experiment, aged rats were used as models to observe the changes of TNFα in plasma and tissue during doxorubicin-induced chronic wound healing. Methods: 24-month-old rats were injected intravenously with doxorubicin 8mg / kg body weight 4 days before the experiment. Then the skin with the diameter of 15cm was resected back to observe the change of TNFα in the wound area and plasma during wound healing. RESULTS: The doxorubicin treatment reduced the wound healing intensity from (868 ± 156) kg / cm2 to (636 ± 136) kg / cm2 in control group (P <005) Wound healing disorders. After the adriamycin attack, the white blood cells decreased to the lowest level on the 7th day and returned to the highest level on the 12th day. At this time, the level of TNFα in the 7th day after adriamycin administration decreased from (0.71 ± 0.68) ng / L to (0.65 ± 0.10) ng / L and (068 ± 0) 15) ng / L, P <005 compared with that before experiment. While the saline control group increased from (0.74 ± 0.10) ng / L before the experiment to 11th day (085 ± 0.12) ng / L (P <005), and the change of leukocyte The trend is similar. The level of TNFα in the adriamycin group was (462 ± 186) ng / g on the 7th day, P <005 compared with that of the control group (995 ± 2.16) ng / g, on the 11th day TNFα in both groups increased, especially in the doxorubicin group (106 ± 112) ng / g, than in the real?