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Skin problems treater Hydrocortisone Acetate

  • Product NameSkin problems treater Hydrocortisone Acetate
    CAS No.50-03-3
    Purity99%
    Min Quantity5000Kilograms
    Price~
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  • CAS No:50-03-3 [2-[(8S,9S,10R,11S,13S,14S,17R)-11,17-dihydroxy-10,13-dimethyl-3-oxo-2,<br />6,7,8,9,11,12,14,15,<br />16-decahydro-1H-cyclopenta[a]phenanthren-17-yl]-2-oxoethyl] acetate
    Molecular Structure

    Detailed Description

    Skin problems treater Hydrocortisone Acetate
    Specializes in skin diseases such as hemorrhoids,
    allergies,rashes,eczema and rheumatoid
    Synonyms: (11beta)-21-(Acetoxy)-11,17,21-trihydroxypregna-1,4-diene-3,20-dione
    CAS:50-03-3
    Molecular Formula: C23H32O6
    Molecular Weight: 404.5
    EINECS: 200-004-4
    Product Implementation Quality Standard: USP,EP
    Chemical Properties: white powder
    Product use: Reducing swelling,itching,and discomfort associated with certain rectal
    conditions,including hemorrhoids.
    keywords: corticosteroid,cortisol,
    gluconeogenesis



    Hydrocortisone acetate suppositories are a topical corticosteroid. It works by depressing the formation,release,and activity of different cells and chemicals that cause swelling,redness,and itching.

    Hydrocortisone(INN,USAN,BAN)is a name for cortisol when it is used as a medication. Hydrocortisone is used to treat people who lack adequate naturally generated cortisol. It is on the World Health Organization's List of Essential Medicines needed in a basic health system.

    Main functions in the body
    Metabolic response
    In the early fasting state,cortisol stimulates gluconeogenesis(the formation of glucose),and activates anti-stress and anti-inflammatory pathways. Cortisol also plays an important,but indirect,role in liver and muscle glycogenolysis,the breaking down of glycogen to glucose-1-phosphate and glucose. This is done through its passive influence on glucagon.

    Additionally,cortisol facilitates the activation of glycogen phosphorylase,which is necessary for epinephrine to have an effect on glycogenolysis.

    In the late fasting state,the function of cortisol changes slightly and increases glycogenesis. This response allows the liver to take up glucose that is not being used by the peripheral tissue and turn it into liver glycogen stores to be used if the body moves into the starvation state.

    Elevated levels of cortisol,if prolonged, can lead to proteolysis(breakdown of proteins)and muscle wasting. Several studies have shown that cortisol can have a lipolytic effect(promote the breakdown of fat). Under some conditions,however, cortisol may somewhat suppress lipolysis.

    Immune response
    Cortisol prevents the release of substances in the body that cause inflammation. It is used to treat conditions resulting from over activity of the B-cell-mediated antibody response. Examples include inflammatory and rheumatoid diseases, as well as allergies. Low-potency hydrocortisone,available as a non-prescription medicine in some countries, is used to treat skin problems such as rashes, and eczema.

    It inhibits production of interleukin(IL)-12,interferon(IFN)-gamma,IFN-alpha and tumor-necrosis-factor(TNF)-alpha by antigen-presenting cells(APCs)and T helper (Th)1 cells,but upregulates IL-4,IL-10,and IL-13 by Th2 cells. This results in a shift toward a Th2 immune response rather than general immunosuppression. The activation of the stress system(and resulting increase in cortisol and Th2 shift)seen during an infection is believed to be a protective mechanism which prevents an over activation of the inflammatory response.

    Cortisol can weaken the activity of the immune system. Cortisol prevents proliferation of T-cells by rendering the interleukin-2 producer T-cells unresponsive to interleukin-1(IL-1),and unable to produce the T-cell growth factor(IL-2). Cortisol also has a negative-feedback effect on interleukin-1.

    Though IL-1 is useful in combating some diseases;however,endotoxic bacteria have gained an advantage by forcing the hypothalamus to increase cortisol levels (forcing the secretion of CRH hormone,thus antagonizing IL-1). The suppressor cells are not affected by glucosteroid response-modifying factor(GRMF),so the effective setpoint for the immune cells may be even higher than the setpoint for physiological processes(reflecting leukocyte redistribution to lymph nodes, bone marrow, and skin). Rapid administration of corticosterone(the endogenous Type I and Type II receptor agonist)or RU28362(a specific Type II receptor agonist)to adrenalectomized animals induced changes in leukocyte distribution. Natural killer cells are affected by cortisol.

    Cortisol stimulates many copper enzymes (often to 50% of their total potential), probably to increase copper availability for immune purposes. This includes lysyl oxidase,an enzyme that cross-links collagen and elastin.Especially valuable for immune response is cortisol's stimulation of the superoxide dismutase,since this copper enzyme is almost certainly used by the body to permit superoxides to poison bacteria.
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  • Skin problems treater Hydrocortisone Acetate
  • Skin problems treater Hydrocortisone Acetate