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P物质的一种代谢产物SP7-11参与炎症性关节疾病的发病机制。

A metabolite of substance P, SP7-11 is involved in the pathogenesis of inflammatory joint disease.

作者信息

Halliday D A, McNeil J D, Scicchitano R

机构信息

Department of Medicine, Royal Adelaide Hospital, South Australia.

出版信息

Med Hypotheses. 1993 Apr;40(4):227-31. doi: 10.1016/0306-9877(93)90046-s.

Abstract

The possibility that neuropeptides, in particular members of the tachykinin family are involved in inflammatory joint disease is widely disputed. Both clinical and experimental observations indicate that the tachykinin substance P (SP) may be involved in the pathogenesis of arthritis. We have studied the effects of tachykinins and the metabolites of SP on chondrocyte function. We have shown that the C-terminal pentapeptide sequence; H-Phe-Phe-Gly-Leu-Met-NH2 is biologically active in bovine chondrocyte cultures. The production of SP7-11 is limited by hydrolysis of the intact peptide by neutral endopeptidase (E.C. 3.4.24.11). The regulation of this enzyme would modulate the activity of substance P on articular cartilage chondrocytes.

摘要

神经肽,尤其是速激肽家族成员参与炎性关节疾病的可能性存在广泛争议。临床和实验观察均表明,速激肽P物质(SP)可能参与关节炎的发病机制。我们研究了速激肽及SP代谢产物对软骨细胞功能的影响。我们已经表明,C末端五肽序列;H-苯丙氨酸-苯丙氨酸-甘氨酸-亮氨酸-甲硫氨酸-氨基在牛软骨细胞培养物中具有生物活性。SP7 - 11的产生受中性内肽酶(E.C. 3.4.24.11)对完整肽的水解作用限制。该酶的调节将调节P物质对关节软骨细胞的活性。

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