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Chemical Compound Review

AC1NSTUL     (4aR,5S,6aS,7S)-5-hydroxy-7- (2...

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Disease relevance of CORTICOSTERONE

  • After 4 d of infusion, dietary intake and weight gain were significantly higher in the Cort and AL groups than in the TNF and TNF+Cort groups [1].
  • We report here that corticosterone (CT) protects cardiomyocytes from apoptotic cell death induced by doxorubicin (Dox), an antineoplastic drug known to induce cardiomyopathy possibly through reactive oxygen species production [2].
  • These data provide support for a specific mode of action for i.c.v. alpha-MSH(1-13), namely blockade of APRs with no impact on acute hyperthermia or increased levels of CORT produced during IS [3].

High impact information on CORTICOSTERONE


Biological context of CORTICOSTERONE


Anatomical context of CORTICOSTERONE

  • The central finding was that the CORT-evoked acceleration of the proliferative response in vitro was attenuated in splenic T cells from animals that had received the high-dose CORT treatment in vivo [9].
  • In the presence of I, A, and C, EGF increased the level of alpha-casein mRNA in pregnant mouse mammary gland explants, but not in rats. kappa-Casein mRNA sequences in mouse mammary gland explants were also significantly increased by EGF in the presence of I, A, and C, but in rat mammary gland explants, the increase was less [10].
  • However, whereas CORT and P4 influenced the ADX-induced increase in the transcription of both types of corticosteroid receptors in the hippocampus, these were unaffected by THP [11].
  • Optic nerve cytosol fractions displayed substantial high-affinity binding of both dexamethasone (DEX) and corticosterone (CORT) that, like GPDH, was elevated approximately two fold in degenerating nerves [12].
  • AS significantly increased UI, adrenal gland weight (AGW), GL, CK activity, and CORT, whereas G. biloba significantly reduced them [13].

Associations of CORTICOSTERONE with other chemical compounds

  • Explants from mammary glands of virgin rats and pregnant rats and mice were cultured under serum-free conditions in the presence of various combinations of the hormones insulin (I), aldosterone (A), corticosterone (C), PRL, and epidermal growth factor (EGF) [10].
  • ICV injections of TRH caused dose-dependent increases in plasma CS, but did not further increase HPA responses when injected together with 5-HT [14].
  • The inhibitory effects of confinement stress or corticosterone (CS) injections on newt sexual behaviors were blocked by pretreatment of newts with mercaptopropionic acid, a blocker of GABA synthesis [5].
  • Replacement with subcutaneous CORT implants (100-mg pellets) for 7 days following ADX rats did not affect CR number, but caused a 38% decrease in GR number compared to control animals (cholesterol-treated, 7-day-ADX rats) [15].
  • The synergy of CORT with T(3) on tadpole tail resorption may depend on the accelerated accumulation of GR transcripts in this tissue during metamorphosis, which may be driven by rising plasma thyroid hormone titers [16].

Gene context of CORTICOSTERONE

  • The ADX + CORT group showed significantly greater increases in both CRH and AVP mRNA levels in the PVN compared to sham rats [17].
  • In repeated stress, the sham groups showed robust increases in PVN CRH and AVP mRNA levels despite high levels of plasma CORT [17].
  • In contrast, in the presence of I, A, C, and PRL, EGF inhibited the induction of both alpha- and kappa-casein mRNA sequences in tissue from rats and mice [10].
  • These data indicate that a CORT-mediated decrease in hippocampal and hypothalamic glucocorticoid receptor mRNA levels is not the only mechanism contributing to the maintenance of a robust HPA response after repeated stress [17].
  • IL-6 bioactivity in serum was not significantly changed by CS treatment, but increased 50 times upon injection of rhIL-1 beta. rhIL-1 beta caused a significantly lower induction of serum IL-6 levels in CS pretreated rats (9-fold) [18].

Analytical, diagnostic and therapeutic context of CORTICOSTERONE

  • Western blot analyses revealed that CT induced an elevation of bcl-xL but not bcl-2 or proapoptotic factors bax, bak, and bad [2].
  • However, the mortality rate was high (> or = 70%) in these experiments and plasma CS elevation persisted in HxCB-treated adrenalectomy survivors [19].
  • Castration failed to reduce the elevation of plasma CS in HxCB-treated male mice [19].
  • Microinjection of ANG II intracerebroventricularly produced a significantly larger increase in AP in Cort-treated rats than in control rats [6].
  • Sixteen female rats were divided into four equal groups (control and 3 experimental groups implanted with tricalcium phosphate lysine drug delivery systems (TCPL) charged with either 50mg selenomethionine (Se), 50 mg corticosterone (C), or 50 mg of both C and Se) [20].


  1. Changes in body composition and dietary intake induced by tumor necrosis factor alpha and corticosterone--individually and in combination. Raina, N., Jeejeebhoy, K.N. Am. J. Clin. Nutr. (1998) [Pubmed]
  2. Corticosteroids inhibit cell death induced by doxorubicin in cardiomyocytes: induction of antiapoptosis, antioxidant, and detoxification genes. Chen, Q.M., Alexander, D., Sun, H., Xie, L., Lin, Y., Terrand, J., Morrissy, S., Purdom, S. Mol. Pharmacol. (2005) [Pubmed]
  3. The long term acute phase-like responses that follow acute stressor exposure are blocked by alpha-melanocyte stimulating hormone. Milligan, E.D., Nguyen, K.T., Deak, T., Hinde, J.L., Fleshner, M., Watkins, L.R., Maier, S.F. Brain Res. (1998) [Pubmed]
  4. Glucocorticoids accelerate anti-T cell receptor-induced T cell growth. Wiegers, G.J., Labeur, M.S., Stec, I.E., Klinkert, W.E., Holsboer, F., Reul, J.M. J. Immunol. (1995) [Pubmed]
  5. Evidence for GABA involvement in stress-induced inhibition of male amphibian sexual behavior. Boyd, S.K., Moore, F.L. Hormones and behavior. (1990) [Pubmed]
  6. Glucocorticoids potentiate central actions of angiotensin to increase arterial pressure. Scheuer, D.A., Bechtold, A.G. Am. J. Physiol. Regul. Integr. Comp. Physiol. (2001) [Pubmed]
  7. Adrenalectomy enhances response of tumour necrosis factor-alpha (TNF-alpha) to haemorrhage in the conscious rat. Yamashita, M., Yamashita, M. Clin. Exp. Immunol. (2001) [Pubmed]
  8. The paraventricular nucleus is uniquely responsive to the feeding stimulatory effects of steroid hormones. Tempel, D.L., Kim, T., Leibowitz, S.F. Brain Res. (1993) [Pubmed]
  9. Long-term in vivo administration of glucocorticoid hormones attenuates their capacity to accelerate in vitro proliferation of rat splenic T cells. Sterzer, P., Wiegers, G.J., Reul, J.M. Endocrinology (2004) [Pubmed]
  10. Bifunctional activity of epidermal growth factor on alpha- and kappa-casein gene expression in rodent mammary glands in vitro. Vonderhaar, B.K., Nakhasi, H.L. Endocrinology (1986) [Pubmed]
  11. The neurosteroid tetrahydroprogesterone attenuates the endocrine response to stress and exerts glucocorticoid-like effects on vasopressin gene transcription in the rat hypothalamus. Patchev, V.K., Hassan, A.H., Holsboer, D.F., Almeida, O.F. Neuropsychopharmacology (1996) [Pubmed]
  12. Evidence for glucocorticoid target cells in the rat optic nerve. Hormone binding and glycerolphosphate dehydrogenase induction. Meyer, J.S., Leveille, P.J., de Vellis, J., Gerlach, J.L., McEwen, B.S. J. Neurochem. (1982) [Pubmed]
  13. Anti-stress effects of Ginkgo biloba and Panax ginseng: a comparative study. Rai, D., Bhatia, G., Sen, T., Palit, G. J. Pharmacol. Sci. (2003) [Pubmed]
  14. Interactions between serotonin, thyrotropin-releasing hormone, and substance P in the CNS regulation of adrenocortical secretion. Saphier, D., Welch, J.E., Farrar, G.E., Nguyen, N.Q., Aguado, F., Thaller, T.R., Knight, D.S. Psychoneuroendocrinology (1994) [Pubmed]
  15. Differential response of type I and type II corticosteroid receptors to changes in plasma steroid level and circadian rhythmicity. Reul, J.M., van den Bosch, F.R., de Kloet, E.R. Neuroendocrinology (1987) [Pubmed]
  16. Developmental expression and hormonal regulation of glucocorticoid and thyroid hormone receptors during metamorphosis in Xenopus laevis. Krain, L.P., Denver, R.J. J. Endocrinol. (2004) [Pubmed]
  17. Increased expression of corticotropin-releasing hormone and vasopressin messenger ribonucleic acid (mRNA) in the hypothalamic paraventricular nucleus during repeated stress: association with reduction in glucocorticoid receptor mRNA levels. Makino, S., Smith, M.A., Gold, P.W. Endocrinology (1995) [Pubmed]
  18. Subchronic glucocorticoid pretreatment reversibly attenuates IL-beta induced fever in rats; IL-6 mRNA is elevated while IL-1 alpha and IL-1 beta mRNAs are suppressed, in the CNS. Chai, Z., Alheim, K., Lundkvist, J., Gatti, S., Bartfai, T. Cytokine (1996) [Pubmed]
  19. Polychlorinated biphenyl-induced immune suppression: castration, but not adrenalectomy or RU 38486 treatment, partially restores the suppressed cytotoxic T lymphocyte response to alloantigen. De Krey, G.K., Baecher-Steppan, L., Deyo, J.A., Smith, B., Kerkvliet, N.I. J. Pharmacol. Exp. Ther. (1993) [Pubmed]
  20. Glomerular response to adrenocortical hormone alone or in combination with selenomethionine. Benghuzzi, H., Tucci, M., Hughes, J., Lyon, R., Adams, S. Biomedical sciences instrumentation. (2005) [Pubmed]
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