Davies J M, Horwitz D A, Davies K J
Department of Medicine, Albany Medical College, New York 12208.
Arthritis Rheum. 1994 Mar;37(3):424-7. doi: 10.1002/art.1780370317.
To study the effects of N-chlorotaurine on collagenase activity, as a model of the effects of neutrophil activation in inflammatory arthritis.
Collagen degradation by collagenase was measured by the release of acid-soluble counts from 3H-collagen.
N-chlorotaurine inhibited the degradation of collagen by bacterial collagenase. This result is explained by a direct inhibition/inactivation of collagenase, since N-chlorotaurine had no effect on the proteolytic susceptibility of collagen itself. The effect appears to be specific to N-chlorotaurine since N-chloroalanine, N-chloroleucine, and HOCl/OCl- failed to inhibit collagenase; in fact, N-chloroalanine and N-chloroleucine actually increased the proteolytic susceptibility of collagen.
N-chlorotaurine may minimize damage to cartilaginous joint structures in inflammatory arthritis by inhibiting/inactivating collagenase.
以中性粒细胞活化在炎性关节炎中的作用为模型，研究N-氯代牛磺酸对胶原酶活性的影响。
通过测量3H-胶原中酸溶性成分的释放来测定胶原酶对胶原的降解作用。
N-氯代牛磺酸抑制细菌胶原酶对胶原的降解。这一结果可通过胶原酶的直接抑制/失活来解释，因为N-氯代牛磺酸对胶原本身的蛋白水解敏感性没有影响。这种作用似乎对N-氯代牛磺酸具有特异性，因为N-氯代丙氨酸(N-chloroalanine)、N-氯代亮氨酸(N-chloroleucine)和次氯酸/次氯酸根未能抑制胶原酶；事实上，N-氯代丙氨酸和N-氯代亮氨酸实际上增加了胶原的蛋白水解敏感性。
N-氯代牛磺酸可能通过抑制/失活胶原酶，使炎性关节炎中软骨关节结构的损伤最小化。
