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NFKB1 Glucocorticoid receptor Transcription factor AP-1 Glucocorticoid receptor Prostaglandin G/H synthase 2 Annexin A1 Cytosolic phospholipase A2 Annexin A1 ATP-binding cassette sub-family A member 1 Solute carrier organic anion transporter family member 1B1 Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 2 Prostaglandin G/H synthase 1 Prostaglandin G/H synthase 2 Thromboxane-A synthase Prostacyclin synthase Prostaglandin E synthase Prostaglandin- H2 D-isomerase Aldo-keto reductase family 1 member C3 Aldo-keto reductase family 1 member C3 Carbonyl reductase [NADPH] 1 Alkaline phosphatase, tissue- nonspecific isozyme Corticosteroid 11-beta- dehydrogenase isozyme 1 Glucocorticoid receptor Glucocorticoid receptor Heat shock protein HSP 90-alpha Heat shock 70 kDa protein 1A/1B Peptidyl-prolyl cis-trans isomerase FKBP4 Heat shock protein HSP 90-alpha Heat shock 70 kDa protein 1A/1B Glucocorticoid receptor Arachidonic acid Prednisolone Prednisolone Prednisolone phosphate Prednisolone phosphate O2 Prostaglandin G2 Prostaglandin H2 H2O Thromboxane A2 Prostaglandin I2 Prostaglandin E2 Prostaglandin D2 NADPH 11-Epi-PGF2a NADP Prostaglandin F2a NADPH NADP PC(18:0/20:4(5Z,8Z,11Z,14Z)) H2O LysoPC(18:0/0:0) Prednisolone phosphate Prednisone Prednisolone Prednisolone Heme Heme Glutathione Prednisolone Prednisolone Acceptor Reduced acceptor Activator Protein 1 NF-kB C/EBP Prostaglandin Synthase G/H 2 Promoter Annexin-1 Peptidyl-prolyl cis-trans isomerase FKBP4 Linoleic Acid Metabolism Eicosanoids Calcium Heme Heme Heme Heme Glucocorticoid receptor-Prednisolone complex binds to the promoter for Annexin-1 (A1) and upregulates the transcription of it. Glucocorticoid receptor-Prednisolone complex inhibits transcription factors NF-kB and Activator Protein 1 (AP-1) from synthesizing prostaglandin G/H synthase 2 (COX-2) Lower concentrations of prostaglanding I2 reduces vasodilation so the swelling of inflammation decreases. Prostaglandin I2 is apart of the hyperalgesia response so it's decrease results in a reduced pain sensitivity. Lower concentrations of prostaglandin D2 decreases the activity of platelet aggregation as well as reducing vasodilation Nucleus Lower concentrations of prostaglandin E2 have similar effects fo PGI2 as it's reduction decreases vasodilation and pain sensitivity. Lower concentrations of prostagladin F2a decreases the amount of bronchoconstriction allowing air to flow more easily. Due to its lipophilicity, prednisolone crosses the cell membrane by passive diffusion Cytoplasm Phospholipase A2 is inhibited by Annexin-1 as it binds to the Ca2+ which is needed by phospholipase A2 to function. This inhibition reduces the amount of arachidonic acid that is cleaved from phospholipids. Lower concentrations of prostaglandin G/H synthase 2 result in the synthesis of prostaglandin G2 and H2 to be reduced. The reduction lowers the amount of prostanoids being produced which have varying effects on decreasing inflammation and immune response. As prednisolone binds to the glucocorticoid receptor, the chaperone proteins fall off. Glucocorticoid receptor-Prednisolone complex translocate into the nucleus. Thromboxane A2 is responsible for activation of new platelets as well as platelet aggravation. Decreased levels of thromboxane A2 will decrease levels of platelet activity. Endoplasmic Reticulum Prostaglandin G/H Synthase 2 exits the nucleus through nuclear pores into the cell cytosol. Liver Human Cell Hepatocytes Endoplasmic reticulum Cytoplasm Blood vessel Blood vessel Prednisolone phosphate is administered orally and opthalmically