Rahman S, Bunning R A, Dobson P R, Evans D B, Chapman K, Jones T H, Brown B L, Russell R G
Department of Human Metabolism and Clinical Biochemistry, University of Sheffield Medical School, UK.
Biochim Biophys Acta. 1992 Apr 30;1135(1):97-102. doi: 10.1016/0167-4889(92)90172-8.
The effect of bradykinin (BK) on proteinase activity, prostaglandin synthesis, and the production of interleukin-6 (IL-6) was investigated in cultures of human osteoblast-like cells. Bradykinin had no effect on stromelysin activity and plasminogen activator activity produced by human osteoblast-like cells. However, BK stimulated the production of prostaglandin E2, an effect that was markedly enhanced by pre-incubation with recombinant interleukin-1 alpha (rhIL-1 alpha), but was apparently unaffected by BK receptor antagonists types 1 and 2. Bradykinin stimulated the intracellular accumulation of total inositol phosphates suggesting that its effects were mediated by stimulation of phosphoinositide metabolism. Bradykinin within the dose range of 10(-11)-10(-5) M also significantly stimulated the production of IL-6. Bradykinin may, therefore, mediate a variety of responses in bone under both physiological and pathological conditions.
在人成骨样细胞培养物中研究了缓激肽（BK）对蛋白酶活性、前列腺素合成以及白细胞介素-6（IL-6）产生的影响。缓激肽对人成骨样细胞产生的基质溶解素活性和纤溶酶原激活剂活性没有影响。然而，BK刺激了前列腺素E2的产生，与重组白细胞介素-1α（rhIL-1α）预孵育可显著增强这一效应，但1型和2型BK受体拮抗剂对其显然没有影响。缓激肽刺激了总肌醇磷酸的细胞内积累，表明其作用是通过刺激磷酸肌醇代谢介导的。在10^(-11)-10^(-5) M剂量范围内的缓激肽也显著刺激了IL-6的产生。因此，缓激肽可能在生理和病理条件下介导骨骼中的多种反应。
