This complex then moves into the nucleus and binds to chromatin, signaling the
production of messenger RNA and coding for enzymes and proteins that determine the response of that particular cell to the hormone.
 
 

1. Constriction of blood vessels and reduction of vascular permeability induced by acute inflammation. This minimizes leakage into the target site of fluid, proteins, and inflammatory cells.
2.  Stabilization of intracellular lysosomal membranes and inhibition of the expression of various damaging enzymes; inhibition of polymorphonuclear (PMN) cell degranulation is also significantly inhibited. 
3. Stabilization of mast cell and basophil membranes is important in inhibiting the process of degranulation and subsequent release of histamine (vasoactive amines), bradykinin, platelet-activating factor (PAF), proteases, and eosinophilic chemotactic factors (ECF). 
4. Mobilization of PMNs from the bone marrow results in neutrophilic leukocytosis. Steroids simultaneously prevent adherence of PMNs to the vascular endothelium, making them less mobile and less accessible to the site of inflammation.
5. Suppression of lymphocyte proliferation and lymphopenia. In small- to moderate-sized doses, corticosteroids more significantly affect T lymphocytes. In larger doses, B lymphocytes are affected as well, and, thus, antibody production.Steroids do not destroy T lymphocytes but rather affect their redistribution into circulation, concentrating them in the bone marrow 
6. Reduction of circulating eosinophils and monocytes. 
7. Inhibition of macrophage recruitment and migration.Steroids also interfere with the ability of macrophages to process antigens. 
8. Suppression of fibroplasia.
9. Depression of the bactericidal activity of monocytes and macrophages. 
10. Via a protein called macrocortin, steroids inhibit phospholipase A2, resulting in inhibition of arachidonic acid degradation and subsequent synthesis of prostaglandins and leukotrienes by cyclooxygenase and lipoxygenase pathways