Leber R, Knecht R, Hasslacher C
Medizinische Universitätsklinik, Heidelberg, Federal Republic of Germany.
Res Exp Med (Berl). 1987;187(5):347-52. doi: 10.1007/BF01855660.
The proteolytic effects of isolated glomeruli of diabetic rats on glomerular basement membrane of nondiabetic rats was investigated at various times after streptozotocin injection. One week after induction of diabetes, proteolytic activity remained unchanged as compared with nondiabetic controls. However, 4 and 10 weeks after streptozotocin injection, glomerular degradation of collagenous (but not noncollagenous) peptides of basement membranes increased (+24% as compared with control experiments). Using diabetic basement membrane as substrate, degradation of collagenous and noncollagenous peptides caused by diabetic glomeruli was 2.6-fold and 1.7-fold higher than in control experiments with nondiabetic glomeruli. The results indicate that the disturbed degradation of glomerular basement membrane in diabetes is not due to a decreased activity of glomerular proteolytic enzymes. In contrast, it can be concluded that the increased resistance of diabetic basement membrane to proteolytic degradation could be partially compensated by quantitative and qualitative changes of the proteolytic potential of diabetic glomeruli.
在注射链脲佐菌素后的不同时间,研究了糖尿病大鼠分离肾小球对非糖尿病大鼠肾小球基底膜的蛋白水解作用。糖尿病诱导一周后,与非糖尿病对照组相比,蛋白水解活性保持不变。然而,在注射链脲佐菌素4周和10周后,基底膜胶原(而非非胶原)肽的肾小球降解增加(与对照实验相比增加24%)。以糖尿病基底膜为底物,糖尿病肾小球引起的胶原和非胶原肽降解比非糖尿病肾小球对照实验高2.6倍和1.7倍。结果表明,糖尿病中肾小球基底膜降解紊乱并非由于肾小球蛋白水解酶活性降低。相反,可以得出结论,糖尿病基底膜对蛋白水解降解的抗性增加可通过糖尿病肾小球蛋白水解潜能的定量和定性变化得到部分补偿。