scholarly journals Bradykinin stimulates bone resorption and lysosomal-enzyme release in cultured mouse calvaria

1984 ◽  
Vol 219 (1) ◽  
pp. 329-332 ◽  
Author(s):  
G T Gustafson ◽  
U Lerner

The effect of bradykinin on bone resorption was studied in cultures of newborn-mouse calvaria. Bradykinin (0.03 microM, 1 microM) stimulated the release of 45Ca2+ from bones dissected out from mice prelabelled in vivo with 45Ca. Bradykinin (1 microM) also augmented the release of stable calcium (40Ca), Pi and the lysosomal enzyme beta-glucuronidase. The stimulatory effect of bradykinin on mineral mobilization and lysosmal -enzyme release could be blocked by indomethacin. It is speculated that concomitant generation of thrombin and bradykinin in areas of trauma and inflammation may induce resorption of nearby bone tissue.

Life Sciences ◽  
1999 ◽  
Vol 65 (18-19) ◽  
pp. 1905-1907 ◽  
Author(s):  
Jana Navarová ◽  
Tatiana Mačičková ◽  
Katarina Horáková ◽  
Miroslava Urbančíková

1988 ◽  
Vol 23 (1) ◽  
pp. 121-128 ◽  
Author(s):  
V. S. Chadwick ◽  
D. M. Mellor ◽  
D. B. Myers ◽  
A. C. Selden ◽  
A. Keshavarzian ◽  
...  

Author(s):  
Vanita Kanase ◽  
Diptesh T Patil

Objective: The aim of this study was to evaluate the in vitro immunomodulatory activity of aqueous and ethanolic extract of dried tubers of Eulophia nuda.Methods: Effect of both the extracts was evaluated at various concentrations (832–6.5 μg/ml) for secretion of mediators such as nitric oxide (NO), superoxide, lysosomal enzyme, and myeloperoxidase activity of isolated murine peritoneal macrophages.Results: The extracts showed stimulation of NO, statistically significant at 832 μg/ml (SI 1.739) for ENA and at 832 μg/ml (stimulation index [SI] 1.662) for ENE; significant stimulation on lysosomal enzyme release for ENA at 832 μg/ml (SI 1.404) and ENE at 832 μg/ml (SI 1.513); myeloperoxidase activity was statistically significant for ENA at 832 μg/ml (SI 1.728) and ENE at 832 μg/ml (SI 1.770).Conclusion: In vitro phagocytic index showed significant results and thus proving the need for confirmation through in vivo studies.


1980 ◽  
Vol 94 (1) ◽  
pp. 138-144 ◽  
Author(s):  
Ulf Lerner

Abstract. The effect of N6-monobutyryl adenosine 3′,5′-cyclic monophosphate (mbcAMP), N6,O2′-dibutyryl adenosine 3′,5′-cyclic monophosphate (dbcAMP), 8-bromo adenosine 3′,5′-cyclic monophosphate (8-brcAMP), adenosine 3′,5′-cyclic monophosphate (cAMP) and two phosphodiesterase (PDE) inhibitors, theophylline and 3-isobutyl-methylxanthine (IBMX) on bone resorption was studied in an organ culture system for 24 h using half calvaria from 6–7 day old mice. The parameters studied were: the release of calcium (Ca2+), inorganic phosphate (Pi), β-glucuronidase, β-galactosidase, lactate dehydrogenase (LDH), and 45Ca from the bones to the medium. With dbcAMP, in concentrations between 5 × 10−5m and 2.5 × 10−4m, and with 8-brcAMP, in concentrations between 10−5m and 5 × 10−5m, a dose-dependent inhibitory effect on the spontaneous release of 45Ca from the explants was found. IBMX and theophylline in doses of 10−3m and 2.5 × 10−3m, respectively, inhibited the spontaneous mobilization of 45Ca, while hypoxanthine, which lacks PDE inhibitory capacity, did not affect the release of 45Ca. When cAMP or its analogues were combined with IBMX, a potentiated inhibitory effect on mineral mobilization and lysosomal enzyme release was seen. In contrast, adenosine 5′-monophosphate, 8-bromo adenosine 5′-monophosphate and sodium butyrate did not reduce the release of 45Ca when applied alone or combined with IBMX. PDE inhibitors combined with parathyroid hormone (PTH) resulted in a reduction of the PTH-stimulated bone resorption. The results provide further evidence that cAMP is not a mediator of the early stage of PTH-induced bone resorption, but on the contrary inhibits mineral mobilization and lysosomal enzyme release from cultured bones.


1985 ◽  
Vol 69 (4) ◽  
pp. 403-411 ◽  
Author(s):  
Keiichi Ohya ◽  
Shoji Yamada ◽  
Rolf Felix ◽  
Herbert Fleisch

1. Bisphosphonates are potent inhibitors of bone resorption and also inhibit prostaglandin (PG) E2 synthesis in bone cells. Therefore we have investigated whether a correlation exists between inhibition of bone resorption and inhibition of PGE2 formation. 2. Initially, bisphosphonates were tested for their effect on the release of [14C]PGE2 from rat calvaria cells labelled with [14C]arachidonic acid and stimulated by bradykinin, thrombin and mechanical manipulation. The effect on [14C]-PGE2 synthesis was not correlated with the known inhibitory activity of bisphosphonates on bone resorption. 3. Mouse calvaria were then treated with epidermal growth factor (EGF) to induce PGE2 synthesis and bone resorption, with or without bisphosphonates. The bisphosphonates either decreased, had no effect or increased PGE2 production, but all inhibited the release of calcium. 4. Finally, the bisphosphonates were given in vivo to mice before explantation of the calvaria. Some of the bisphosphonates decreased the production of PGE2, suggesting that these compounds may have such an effect in vivo. But again no relationship between the effect on PGE2 synthesis and bone resorption was found. 5. Thus, these experiments show the inhibitory effect of bisphosphonates on bone resorption is unlikely to be explained only by their effect on PGE2 synthesis.


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