Fluocinonide¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Fluocinonide is a potent glucocorticoid steroid used topically as anti-inflammatory agent for the treatment of skin disorders such as eczema. It relieves itching, redness, dryness, crusting, scaling, inflammation, and discomfort. Fluocinonide binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. Cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In another words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Like other glucocorticoid agents Fluocinolone acetonide acts as a physiological antagonist to insulin by decreasing glycogenesis (formation of glycogen). It also promotes the breakdown of lipids (lipolysis), and proteins, leading to the mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating glucose concentrations (in the blood). There is also decreased glycogen formation in the liver. Gentamicin¿¡ ´ëÇÑ Mechanism_Of_Action Á¤º¸ Aminoglycosides like gentamicin "irreversibly" bind to specific 30S-subunit proteins and 16S rRNA. Specifically gentamicin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.
Pharmacology
Fluocinonide¿¡ ´ëÇÑ Pharmacology Á¤º¸ Fluocinonide is a potent glucocorticoid steroid used topically as anti-inflammatory agent for the treatment of skin disorders such as eczema. It relieves itching, redness, dryness, crusting, scaling, inflammation, and discomfort. [Wikipedia] Gentamicin¿¡ ´ëÇÑ Pharmacology Á¤º¸ Gentamicin is a broad spectrum aminoglycoside antibiotic. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses.
Fluocinonide¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Not Available Gentamicin¿¡ ´ëÇÑ ´Ü¹é°áÇÕ Á¤º¸ Low (between 0 and 30%)
Half-life
Fluocinonide¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ Not Available Gentamicin¿¡ ´ëÇÑ ¹Ý°¨±â Á¤º¸ 3-3¨ö hours in infants one week to six months of age; this increases to 5¨ö hours in full-term and large premature infants less than one week old.
Absorption
Fluocinonide¿¡ ´ëÇÑ Absorption Á¤º¸ The extent of percutaneous absorption of topical corticosteroids is determined by many factors including the vehicle, the integrity of the epidermal barrier, and the use of occlusive dressings. Gentamicin¿¡ ´ëÇÑ Absorption Á¤º¸ Injections lead to peak serum concentrations in 30-60 minutes. Topical gentamicin is readily absorbed from large burned, denuded, or granulating areas but not through intact skin. Absorption of gentamicin is faster and greater with the cream compared to the ointment. Gentamicin is absorbed in small quantities following topical application to the eye. Gentamicin is also absorbed in small amounts following topical application to the ear (especially if the eardrum is perforated or if tissue damage is present).
Fluocinonide¿¡ ´ëÇÑ Toxicity Á¤º¸ Side effects may include acne-like eruptions, burning, dryness, excessive hair growth, infection of the skin, irritation, itching, lack of skin color, prickly heat, skin inflammation, skin loss or softening, stretch marks Gentamicin¿¡ ´ëÇÑ Toxicity Á¤º¸ Mouse, intravenous LD50: 52 mg/kg; rat, intravenous LD50: 96 mg/kg.
Drug Interactions
Fluocinonide¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Not Available Gentamicin¿¡ ´ëÇÑ Drug_Interactions Á¤º¸ Atracurium The agent increases the effect of muscle relaxantDoxacurium The agent increases the effect of muscle relaxantGallamine Triethiodide The agent increases the effect of muscle relaxantMetocurine The agent increases the effect of muscle relaxantMivacurium The agent increases the effect of muscle relaxantPancuronium The agent increases the effect of muscle relaxantPipecuronium The agent increases the effect of muscle relaxantRocuronium The agent increases the effect of muscle relaxantSuccinylcholine The agent increases the effect of muscle relaxantTubocurarine The agent increases the effect of muscle relaxantVecuronium The agent increases the effect of muscle relaxantBumetanide Increased ototoxicityEthacrynic acid Increased ototoxicityFurosemide Increased ototoxicityTorasemide Increased ototoxicityThalidomide Thalidomide increases the renal toxicity of the aminoglycosideCisplatin Increased risk of nephrotoxicityCefradine Increased risk of nephrotoxicityCephapirin Increased risk of nephrotoxicityCefamandole Increased risk of nephrotoxicityCefazolin Increased risk of nephrotoxicityCefonicid Increased risk of nephrotoxicityCefoperazone Increased risk of nephrotoxicityCeforanide Increased risk of nephrotoxicityCefotaxime Increased risk of nephrotoxicityCefotetan Increased risk of nephrotoxicityCefoxitin Increased risk of nephrotoxicityCeftazidime Increased risk of nephrotoxicityCeftizoxime Increased risk of nephrotoxicityCeftriaxone Increased risk of nephrotoxicityCefuroxime Increased risk of nephrotoxicityCephalothin Group Increased risk of nephrotoxicity
Fluocinonide¿¡ ´ëÇÑ Description Á¤º¸ A topical glucocorticoid used in the treatment of eczema. [PubChem] Gentamicin¿¡ ´ëÇÑ Description Á¤º¸ A complex of three different closely related aminoglycoside sulfates, Gentamicins C1, C2, and C1(subA), obtained from Micromonospora purpurea and related species. They are broad-spectrum antibiotics, but may cause ear and kidney damage. They act to inhibit protein synthesis (genetic translation). [PubChem]
Fluocinonide¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ Not Available Gentamicin¿¡ ´ëÇÑ Chemical_IUPAC_Name Á¤º¸ 2-[4,6-diamino-3-[3-amino-6-(1-methylaminoethyl)oxan-2-yl]oxy-2-hydroxycyclohexyl]oxy-5-methyl-4-methylaminooxane-3,5-diol
Drug-Induced Toxicity Related Proteins
GENTAMICIN ÀÇ Drug-Induced Toxicity Related ProteinÁ¤º¸ Replated Protein:Phospholipase A Drug:gentamicin Toxicity:aminoglycoside toxicity. [¹Ù·Î°¡±â]Replated Protein:phospholipases C Drug:gentamicin Toxicity:aminoglycoside toxicity. [¹Ù·Î°¡±â]Replated Protein:Angiotensinase A Drug:gentamicin Toxicity:important consequences upon renal function and metabolism. [¹Ù·Î°¡±â]Replated Protein:Dipeptidylpeptidase IV Drug:gentamicin Toxicity:important consequences upon renal function and metabolism. [¹Ù·Î°¡±â]Replated Protein:Sodium/potassium-transporting ATPase Drug:Gentamicin Toxicity:necrosis. [¹Ù·Î°¡±â]