Effects of smoking on the wound healing of stage 4 pressure ulcers in rats
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摘要: 目的 探讨吸烟对大鼠4期压疮创面愈合的影响。 方法 取50只6~8周龄雄性SD大鼠,按随机数字表法分为单纯压疮组和吸烟+压疮组,每组25只。吸烟+压疮组大鼠接受12周被动吸烟干预后,2组大鼠均于背部肌肉内放置铁片,铁片对应位置皮肤外放置磁铁加压,每次2 h,每天5次,连续加压6 d建立4期压疮模型。在造模后即刻,每组取3只大鼠处死后取创面组织,苏木精-伊红染色观察创面组织病理学改变。造模后1、3、7、14 d,每组各取3只大鼠,用卡纸法测量压疮创面面积;创面面积测量后处死大鼠取创面组织,采用免疫组织化学法检测创面组织基质金属蛋白酶9(MMP-9)、组织金属蛋白酶抑制物1(TIMP-1)蛋白表达水平,并计算MMP-9/TIMP-1比值。记录2组剩余各10只大鼠的创面愈合时间。对数据进行析因设计方差分析、两独立样本
t 检验及Bonferroni校正。 结果 (1)造模后即刻,单纯压疮组大鼠创面可见大面积肌纤维坏死溶解,肌原纤维排列疏松,周围可见较多的淋巴细胞以及单核细胞浸润。吸烟+压疮组大鼠创面可见大量坏死肌纤维溶解并逐渐消失,肌原纤维排列疏松,弥漫性淋巴细胞以及单核细胞浸润数量明显多于单纯压疮组。(2)吸烟+压疮组大鼠造模后1、3、7、14 d创面面积均明显大于单纯压疮组(t =3.019、2.549、2.181、3.674,P <0.05或P <0.01)。(3)造模后1~14 d,2组大鼠创面组织MMP-9、TIMP-1的蛋白表达水平和MMP-9/TIMP-1比值均呈先上升后下降的趋势。造模后1、3、7、14 d,吸烟+压疮组大鼠创面组织MMP-9蛋白表达水平和MMP-9/TIMP-1比值明显高于单纯压疮组(t =4.783、4.508、6.325、7.204,3.078、2.989、4.081、4.696,P <0.05或P <0.01);2组大鼠创面组织TIMP-1蛋白表达水平相近。(4)吸烟+压疮组大鼠创面愈合时间为(48.9±2.6)d,明显长于单纯压疮组的(35.2±2.3)d(t =12.477,P <0.05)。 结论 吸烟通过上调压疮创面中MMP-9的表达,导致MMP-9/TIMP-1比值失衡,从而影响大鼠4期压疮创面的愈合。-
关键词:
- 伤口愈合 /
- 压力性溃疡 /
- 吸烟 /
- 基质金属蛋白酶9 /
- 基质金属蛋白酶抑制剂1
Abstract: Objective To explore the effect of smoking on the wound healing of stage 4 pressure ulcers in rats. Methods Fifty male Sprague-Dawley rats aged 6-8 weeks were divided into simple pressure ulcer group and smoking+ pressure ulcer group according to the random number table, with 25 rats in each group. After the rats in the smoking+ pressure ulcer group received passive smoking intervention for 12 weeks, an iron plate was placed in the back muscle of each rat in 2 groups, and a magnet was placed outside the skin at the corresponding position of the iron plate for 2 h at each time, with 5 times a day and continuously for 6 days to reproduce stage 4 pressure ulcer model. Immediately after establishing the model, 3 rats in each group were sacrificed and wound tissue was collected, and hematoxylin-eosin staining was applied to observe the pathological changes of the wounds. On 1, 3, 7, and 14 day (s) after establishing the model, 3 rats in each group were collected to measure the pressure ulcer wound area by the paper jam method. After measurement of the wound area, the rats were sacrificed and the wound tissue was collected, and the protein expression levels of matrix metalloproteinases 9 (MMP-9) and tissue inhibitor of metalloproteinase 1 (TIMP-1) in wound tissue were detected by immunohistochemical method, and the ratio of MMP-9/TIMP-1 was calculated.The wound healing time of the remaining 10 rats in each group was recorded. Data were statistically analyzed with analysis of variance for factorial design, two independent samplet test, and Bonferroni correction. Results (1) Immediately after establishing the model, muscle fiber necrosis and dissolution with large areas were seen on the wound, the myofibrils arranged loosely, and more lymphocytes and monocytes infiltration were seen around the wound of rats in simple pressure ulcer group. A large number of necrotic myofibers were dissolved and gradually disappeared, the myofibrils arranged loosely, and the number of diffuse lymphocytes and monocyte infiltration in wound of rats in smoking+ pressure ulcer group were significantly higher than those in simple pressure ulcer group. (2) The wound areas of rats in smoking+ pressure ulcer group were significantly larger than those in simple pressure ulcer group on 1, 3, 7, and 14 day (s) after establishing the model (t =3.019, 2.549, 2.181, 3.674,P <0.05 orP <0.01). (3) On 1 to 14 days after establishing the model, the protein expression levels of MMP-9 and TIMP-1 in the wound tissue and the ratio of MMP-9/TIMP-1 of rats in the two groups increased first and then decreased. On 1, 3, 7, and 14 day (s) after establishing the model, the protein expression levels of MMP-9 in the wound tissue and the ratio of MMP-9/TIMP-1 of rats in smoking+ pressure ulcer group were significantly higher than those in simple pressure ulcer group (t =4.783, 4.508, 6.325, 7.204, 3.078, 2.989, 4.081, 4.696,P <0.05 orP <0.01), and the protein expression levels of TIMP-1 in wound tissue of rats in the two groups were similar. (4) The wound healing time of rats in smoking+ pressure ulcer group was (48.9±2.6) d, which was significantly longer than (35.2±2.3) d of simple pressure ulcer group (t =12.477,P <0.05). Conclusions Smoking can up-regulate the expression of MMP-9 in pressure ulcer wound and result in an imbalance of MMP-9/TIMP-1, thereby affecting the wound healing of stage 4 pressure ulcers in rats.
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