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目的:观察生肌玉红胶原的抑菌与调控创面金属蛋白酶而促进慢性创面愈合的作用机制。方法:采用试管法与平皿法实验以评估生肌玉红胶原强度,以大鼠感染性创面测定创面肉芽组织中羟脯氨酸、MMPs(MMP-1、MMP-2、MMP-9)含量,以电子照相法采用Image J软件分析测定创面面积。结果:生肌玉红胶原显著抑制外科临床常见细菌与耐药菌生长,对各种细菌的最小抑菌浓度为0.25 g/m L,抑菌范围为10.5~19.5 mm;在大鼠感染性慢性创面造模后3d起生肌玉红胶原显著抑制创面肉芽MMP1、MMP2及MMP9含量(P<0.01),其中以MMP9表达影响疗效最显著;在造模后第7、15天生肌玉红胶原组创面羟脯氨酸含量显著高于对照组与胶原组(P<0.05)。造模后第3~15天,生肌玉红胶原组创面面积显著小于对照组与胶原组(P<0.05),造模后15 d,胶原组创面面积亦显著小于对照组(P<0.05)。结论:生肌玉红胶原通过抑制外科临床常见细菌与耐药菌感染,降低创面金属蛋白酶分泌,促进肉芽羟脯氨酸合成而加速慢性创面愈合。
Objective: To observe the mechanism of myogenic jade red collagen inhibition of bacteria and the regulation of the wound surface metalloproteinases and promote chronic wound healing. Methods: In vitro and in vivo experiments were conducted to evaluate the intensity of myogenic jade red collagen. The levels of hydroxyproline and MMPs (MMP-1, MMP-2, MMP-9) The area of the wound was analyzed by Image J software by electrophotography. Results: Mycoplasma jade red collagen significantly inhibited the growth of common clinical and resistant bacteria in clinical practice. The minimum inhibitory concentration (MIC) of all bacteria was 0.25 g / m L and the range of inhibition ranged from 10.5 to 19.5 mm. After 3 days, the myogenic jade red collagen significantly inhibited the expression of MMP1, MMP2 and MMP9 in wound granulation (P <0.01), of which the most significant effect was MMP9 expression. On the 7th and 15th day after operation, The content of hydroxyproline in the wound surface was significantly higher than that in the control group and the collagen group (P <0.05). On the 3rd to 15th day after modeling, the wound area of myogenic jade red collagen group was significantly smaller than that of the control group and the collagen group (P <0.05), and the wound surface area of the collagen group was also significantly less than that of the control group 15 days after model establishment (P <0.05) . CONCLUSION: Myogenic jade red collagen accelerates the healing of chronic wounds by inhibiting bacterial and drug-resistant bacterial infections in clinical practice, reducing the secretion of metalloproteinase and promoting hydroxyproline synthesis in granulation tissue.