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Biphasic enhacement of nitric oxide synthase activity and cGMP level following brain ischemia in gerbils

100%

Strosznajder J., Chalimoniuk M.

Acta Neurobiologiae Experimentalis

1996

vol. 56

issue 1

71-81

This study was aimed to examine properties and changes in nitric oxide synthase (NOS) activity and cGMP level during reperfusion after 5 min of brain ischemia in gerbils. Animals were treated 5 min befor ischemia with NOS inhibitors: N-nitro-L-arginine (NNLA), or 7-Nitroindazole (7-NI), or with the inhibitor of guanylate cyclase, LY 83583, or with hydrocortisone for 7 days before ischemia. Northern bolt analysis was performed using specific cDNA for inducible NOS. It was observed that ischemia significantly enhances NOS activity and cGMP level. During reperfusion, biphasic increase in NOS activity and cGMP level took place with two peaks 15 min and 2 h after ischemia. NNLA, 7-NI, and LY 83583 eliminated enhancements of NOS activity and cGMP level, whereas glucocorticoid remained without effect. There was no activation of gene encoding inducible NOS (iNOS). Our results indicate that ischemia-reperfusion activates constitutive NOS. It is suggested that nitric oxide (NO) production during reperfusion is related to neuronal degeneration and that inhibitor of NOS offers a new therapeutical strategies.

Suppression of mast cell activation by glucocorticoid

88%

Yoshikawa H., Tasaka K.

vol. 48

issue 5

487-496

Mast cells play a critical role in allergic diseases. When mast cells are activated by cross-linking of their high affinity IgE receptors by the antigen and IgE antibodies, release of chemical mediators is followed by secretion of multiple cytokines. We report that IL-3-dependent mucosal-type mast cells undergo apoptosis when IL-3 is withdrawn. In addition, cross-linking of high affinityIgE receptors prevents apoptosis of mast cells by paractine mechanisms, producing IL-3, IL-4 and granulocyte/macrophage colony-stimulating factor (GM-CSF). However, the secretion of endogenous growth factors are not enough for cell survival, whereas IL-4 induces cell aggregation by expressing adhesion molecules such as leukocyte function-associated antigen 1 (LFA-1), and makes it reactive to endogenous growth factors by contact cell to cell interaction. On the other hand, dexamethazone down-regulates the expression of intracellular adhesion molecule 1 (ICAM-1) and IL-4 in activated mast cells, by which the self-aggregation of mast cells is inhibited and poptosis is induced. Thus, glucocorticoids suppress mast cell survival by inhibiting IL-4 production and expression of adhesion molecules.

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1 Acta Neurobiologiae Experimentalis

1 Archivum Immunologiae et Therapiae Experimentalis

1 2000

1 1996

1 Chalimoniuk M.

1 Strosznajder J.

1 Tasaka K.

1 Yoshikawa H.

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Biphasic enhacement of nitric oxide synthase activity and cGMP level following brain ischemia in gerbils

Suppression of mast cell activation by glucocorticoid