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目的探讨糖尿病足筋疽(肌腱坏死症)肌腱“隐性病变”的发病机制。方法腹腔一次性注射链脲佐菌素(STZ)复制Wistar大鼠糖尿病模型,动态观察成模大鼠体重、血糖;定期处死大鼠,检测后爪部肌腱组织病理、超微结构及组织糖、糖基化终产物(AGEs)、羟脯氨酸(Hyp)、髓过氧化物酶(MPO)变化。结果模型各组肌腱组织病理及超微结构、组织糖、AGEs、Hyp、MPO均有不同程度的改变。随着时间延长,肌腱组织病理及超微结构组织损害程度持续加重;组织糖、AGEs、MPO呈逐渐上升趋势,而Hyp呈逐渐下降趋势,与正常组比较,有统计学差异(P<0.05～P<0.01)。结论糖尿病模型大鼠后肢肌腱组织早期即出现隐性病理损害;其机制可能与肌腱组织糖含量升高、蛋白非酶糖化、肌腱基质病理改变和炎症反应等有关。
Objective To investigate the pathogenesis of tendinosis in patients with diabetic foot gangrene (tendon necrosis). Methods The diabetic model of Wistar rats was injected intraperitoneally with streptozotocin (STZ). The body weight and blood glucose of the model rats were dynamically observed. The rats were sacrificed on a regular basis. The pathological, ultrastructural, Glycosylation end products (AGEs), hydroxyproline (Hyp), myeloperoxidase (MPO) changes. Results The pathological and ultrastructural changes of tendon tissue, tissue glucose, AGEs, Hyp and MPO in different groups were all changed to some extent. With the prolongation of time, the pathological and ultrastructural damage of tendon continued to worsen. The levels of carbohydrate, AGEs and MPO increased gradually while Hyp gradually decreased. Compared with the normal group, there was a significant difference (P <0.05 ~ P <0.01). CONCLUSION: The pathological changes of tibia and tendon in early diabetic rats are occult pathological changes. The possible mechanism may be related to the increase of carbohydrate content, non-enzymatic glycation of protein, pathological change of tendon matrix and inflammatory reaction in tendon tissue.