目的 探讨消肿止痛合剂（Xiaozhong Zhitong Mixture， XZZT）通过AMPK /SIRT1/NF-κB信号通路对糖尿病溃疡大鼠氧化应激和炎症损伤的影响。 方法 将100只SPF级雄性SD大鼠随机分为空白（Control）组、模型（Model）组、消肿止痛合剂（XZZT）组、AMPK抑制剂（CC）组、消肿止痛合剂 + AMPK抑制剂（XZZT + CC）组，除Control组外，其余各组均通过高脂高糖饲养、腹腔注射链脲佐菌素和皮肤缺损法建立糖尿病溃疡模型大鼠。成模后，XZZT组与XZZT + CC组给予消肿止痛合剂1 mL/（100 g·d）灌胃；Control组、Model组和CC组予以等体积0.9%氯化钠注射液灌胃，每天1次；CC组和XZZT + CC组一次性腹腔注射0.2 mg/kg AMPK抑制剂Compound C，于干预后第7、14天取材。观察创面大体情况，测量创面面积，计算创面愈合率；采用苏木素-伊红（HE）染色法检测创面肉芽组织病理变化；采用酶联免疫吸附测定法（ELISA）检测创面组织中白细胞介素-6（IL-6）、白细胞介素-10（IL-10）、肿瘤坏死因子-α（TNF-α）水平；采用硫代巴比妥酸法测定丙二醛（MDA）含量，羟胺法测定超氧化物歧化酶（SOD）活性；Western blot方法检测创面组织中AMPK、磷酸化AMPK（p-AMPK）、SIRT1、NF-κB、磷酸化NF-κB（p-NF-κB）蛋白表达水平；RT-qPCR检测AMPK、SIRT1、IL-6、TNF-α mRNA表达水平。 结果 与Control组相比，Model组在治疗后的第7、14天IL-6、TNF-α水平、MDA含量、p-NF-κB蛋白表达及IL-6、TNF-α mRNA表达水平升高，IL-10水平、SOD活性、p-AMPK/AMPK值和SIRT1 mRNA及蛋白表达水平降低（P < 0.01）；与Model组相比，XZZT组创面愈合率、IL-10、SOD、p-AMPK/AMPK值、SIRT1 mRNA及蛋白表达水平升高，IL-6、TNF-α、MDA、p-NF-κB蛋白表达及IL-6、TNF-αmRNA水平降低（P < 0.01）；而CC组呈现相反趋势（P < 0.05）；与XZZT组相比，XZZT + CC组IL-6、TNF-α、MDA、p-NF-κB蛋白表达及IL-6、TNF-α mRNA表达水平升高，创面愈合率、IL-10、SOD活性、p-AMPK/AMPK值和SIRT1 mRNA及蛋白表达水平降低（P < 0.01）。 结论 XZZT可能通过激活AMPK/SIRT1信号通路，抑制NF-κB磷酸化，有效减轻糖尿病溃疡大鼠的氧化应激和炎症损伤，加速糖尿病溃疡愈合。

Objective To investigate the effects of Xiaozhong Zhitong Mixture （XZZT） on oxidative stress and inflammatory injury in rats with diabetic ulcers through the AMPK/SIRT1/NF-κB signaling pathway. Methods A total of one hundred specific-pathogen-free （SPF）-grade male sprague-dawley （SD） rats were randomly allocated into five groups： a control group， a model group， an XZZT group， an AMP-activated protein kinase （AMPK） inhibitor （Compound C， CC） group， and an XZZT + CC group. Except for the rats in the control group， diabetic ulcer models were established through a high-fat and high-sugar diet， intraperitoneal injection of streptozotocin， and full-thickness skin excision. After successful model establishment， the rats in the XZZT and XZZT + CC groups were administered XZZT via gavage at a dosage of 1 mL/（100 g·d）， whereas the rats in the control， model， and CC groups received an equal volume of 0.9% sodium chloride solution once daily. The rats in the CC and XZZT + CC groups were intraperitoneally injected with 0.2 mg/kg of the AMPK inhibitor Compound C once. Tissue samples were collected on the 7th and 14th days after the intervention. The wound conditions were observed， the wound area was measured， and the healing rate was calculated. Hematoxylin-eosin （HE） staining was employed to examine the pathological changes in the granulation tissue. Enzyme-linked immunosorbent assay （ELISA） was conducted to detect the levels of interleukin-6 （IL-6）， interleukin-10 （IL-10）， and tumor necrosis factor-α （TNF-α） in the wound tissues. The malondialdehyde （MDA） content was measured using the thiobarbituric acid method， and the superoxide dismutase （SOD） activity was determined by the hydroxylamine method. Western blot analysis was utilized to assess the protein expression of AMPK， phosphorylated AMPK （p-AMPK）， sirtuin 1 （SIRT1）， nuclear factor-kappa B （NF-κB）， and phosphorylated NF-κB （p-NF-κB）. Reverse transcription-quantitative polymerase chain reaction （RT-qPCR） was applied to measure the mRNA expression levels of AMPK， SIRT1， IL-6， and TNF-α. Results When compared to the control group， the model group demonstrated elevated levels of IL-6， TNF-α， MDA， p-NF-κB protein， as well as IL-6 and TNF-α mRNA， accompanied by a decrease in the IL-10 level， SOD activity， p-AMPK/AMPK ratio， and SIRT1 mRNA and protein expression on days 7 and 14 （P < 0.01）. In comparison with the model group， the XZZT group presented a higher wound healing rate， IL-10 level， SOD activity， p-AMPK/AMPK ratio， and SIRT1 mRNA and protein expression， along with lower levels of IL-6， TNF-α， MDA， p-NF-κB protein， and IL-6 and TNF-α mRNA （P < 0.01）. Conversely， the CC group exhibited opposite trends （P < 0.05）. When compared to the XZZT group， the XZZT + CC group showed increased levels of IL-6， TNF-α， MDA， p-NF-κB protein， and IL-6 and TNF-α mRNA， and a reduced wound healing rate， IL-10 level， SOD activity， p-AMPK/AMPK ratio， and SIRT1 mRNA and protein expression （P < 0.01）. Conclusion Xiaozhong Zhitong Mixture may alleviate oxidative stress and inflammatory injury， thereby accelerating diabetic ulcer healing in rats. This effect is possibly achieved by activating the AMPK/SIRT1 signaling pathway and suppressing NF-κB phosphorylation.