Pathways

Metabolites of Prednisolone phosphate are predicted with biotransformer.

Prednisone is a medication that is used to suppress the immune system. It works by interrupting cytokine pathways type 1 and type 2. It is administered orally, through tablet, or solution (concentrated or non-concentrated). Prednisone is a glucocorticoid, and as well as being used for immune system suppression, it is used for its anti inflammatory properties. It exerts these properties by binding to glucocorticoid receptors in the cell, which inhibits inflammatory cells. This prevents inflammatory mediators from being expressed.

Prednisone is a corticosteroid used to treat inflammation or immune-mediated reactions and to treat endocrine or neoplastic diseases. It is indicated as an anti-inflammatory or immunosuppressive drug for allergic, dermatologic, gastrointestinal, hematologic, ophthalmologic, nervous system, renal, respiratory, rheumatologic, infectious, endocrine, or neoplastic conditions as well as in organ transplant. It is derived from cortisone.1 It is biologically inert and converted to prednisolone in the liver by the enzyme Corticosteroid 11-beta-dehydrogenase isozyme 1. As prednisolone is a glucocorticoid, it's mechanism of actions is that of the glucocorticoid response element of influencing COX-2/prostaglandin G/H synthase 2 suppression and lipocortin/annexin induction. By binding to the glucocorticoid receptor, it influences transcription factors AP-1 and NF-kB to block the transcription of COX-2/prostaglandin G/H synthase 2 which reduces the amount of prostanoids being produced from arachidonic acid. Prostanoids such as PGI2 and thromboxane A2 influence effects of inflammation through vasoconstriction/dilation, pain sensitivity and platelet aggregation. Prednisolone also affects the promoter of annexin-1, an important inflammatory protein as it affects leukocytes and blocks phospholipase A2 which reduces the amount of arachidonic acid being cleaved from the phospholipid bilayer. Reducing the amount of arachidonic acid formed further decreases concentrations of prostanoids mentioned calming inflammation.

Prednisone is a medication that is used to suppress the immune system. It works by interrupting cytokine pathways type 1 and type 2. It is administered orally, through tablet, or solution (concentrated or non-concentrated). Prednisone is a glucocorticoid, and as well as being used for immune system suppression, it is used for its anti inflammatory properties. It exerts these properties by binding to glucocorticoid receptors in the cell, which inhibits inflammatory cells. This prevents inflammatory mediators from being expressed.

Prednisone is a synthetic, anti-inflammatory glucocorticoid that derives from cortisone. It is biologically inert and converted to prednisolone in the liver. The glucocorticoid receptor is located intracellularly within the cytoplasm and, upon binding, trans-locates rapidly into the nucleus, where it affects gene transcription and causes inhibition of gene expression and translation for inflammatory leukocytes and structural cells such as epithelium.

Pregabalin is an anticonvulsant drug used to treat neuropathic pain conditions and fibromyalgia, and for the treatment of partial onset seizures in combination with other anticonvulsants. Pregabalin is structurally similar to gamma-aminobutyric acid (GABA) - an inhibitory neurotransmitter. Its properties include anxiolytic, anticonvulsant and analgesic effects. Although the structure of pregabalin is similar to gamma-aminobutyric acid (GABA), it does not bind to GABA receptors. Instead, it binds the alpha2-delta subunit of presynaptic voltage-gated calcium channels in the central nervous system. Pregabalin does not modulate dopamine receptors, serotonin receptors, opiate receptors, sodium channels or cyclooxygenase activity. In glutamatergic neurons, glutamate is synthesized from the amino acid glutamine and transported into synaptic vesicles by excitatory amino acid transporter and stored until an action potential arrives at the nerve terminal. When an action potential does arrive at the nerve terminal, this triggers the opening of voltage gated L-type calcium channel, leading to the influx of calcium ions into the presynaptic nerve terminal. The influx of calcium triggers the release of the stored neurotransmitter into the synapse via exocytosis. Glutamate is an excitatory neurotransmitter, thus, once it gets in the synapse it activates NMDA and AMPA receptors. Activation of NMDA receptors results in calcium ions being transported into the post synaptic neuron. Activation of AMPA receptor results in sodium being transported into the post synaptic neuron. The influx of cations into the post synaptic neuron leads to depolarization/ excitation of the neuron. Pregabalin inhibits subunit alpha-2/delta-1 of the voltage gated L-type calcium channel. This prevents the influx of calcium ions when an action potential arrives at the nerve terminal. With low calcium concentration in the presynaptic neuron, excitatory neurotransmitters like glutamate cannot be released and thus the electrical signal is terminated. This is beneficial in conditions like seizures, to prevent the uncontrolled electrical activity that occurs in the brain during an epileptic episode. Pregabalin is an oral drug administered in the fasted state, pregabalin absorption is rapid, and extensive. Common side effects of taking pregabalin include drowsiness, dizziness, blurred vision, difficulty with concentration/attention, dry mouth, edema, and weight gain. Following rapid or abrupt discontinuation of pregabalin, some patients reported symptoms including insomnia, nausea, headache, anxiety, nervousness, irritability, hyperhidrosis, and diarrhea. Chronic use of pregabalin can result in physical dependence, and there is a risk of abuse associated with its use, especially in patients on opioid medicines or who have a history of substance abuse.