Kucharz E
Med Interne. 1984 Apr-Jun;22(2):129-40.
Collagen metabolism was studied in patients with viral hepatitis, chronic hepatic disorders as well as under experimental conditions, in rats with carbon tetrachloride-induced hepatic fibrosis. Changes in serum hydroxyproline, hydroxylysine and collagen-like protein levels, and collagen peptidase activity were observed in clinical investigations. An increase of collagen content and collagen-glycosaminoglycan interactions were found in the liver samples of rats with the hepatic fibrosis. An increase of collagenase activity in the course of fibrosis is due to an elevated biosynthesis of the enzyme de novo as well as to a decreased content of inhibitors. The activity of collagen peptidase and collagenolytic cathepsin were increased, and it was suggested that an increase of collagen degradation in the liver was a self-defensive mechanism against fibrosis but insufficient to protect the organ against it. This was caused probably by changes in susceptibility of collagen to degradating enzymes in the course of chronic hepatic disorders.
在病毒性肝炎、慢性肝脏疾病患者以及在实验条件下，对四氯化碳诱导肝纤维化的大鼠的胶原代谢进行了研究。临床研究中观察到血清羟脯氨酸、羟赖氨酸和胶原样蛋白水平以及胶原肽酶活性的变化。在肝纤维化大鼠的肝脏样本中发现胶原含量增加以及胶原与糖胺聚糖的相互作用增强。纤维化过程中胶原酶活性的增加是由于该酶从头生物合成增加以及抑制剂含量降低。胶原肽酶和胶原olytic组织蛋白酶的活性增加，并且有人提出肝脏中胶原降解的增加是针对纤维化的一种自我防御机制，但不足以保护器官免受其害。这可能是由于慢性肝脏疾病过程中胶原对降解酶的敏感性发生了变化。
