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Corticosterone

$64

Brand : BIOFRON
Catalogue Number : BN-O0045
Specification : 98%(HPLC)
CAS number : 50-22-6
Formula : C21H30O4
Molecular Weight : 346.46
PUBCHEM ID : 5753
Volume : 20mg

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Catalogue Number

BN-O0045

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

346.46

Appearance

Powder

Botanical Source

Structure Type

Category

Standards;Natural Pytochemical;API

SMILES

CC12CCC(=O)C=C1CCC3C2C(CC4(C3CCC4C(=O)CO)C)O

Synonyms

Pregn-4-ene-3,20-dione, 11β,21-dihydroxy-/CORTICOSTERONE/Pregn-4-ene-3,20-dione, 11β, 21-dihydroxy-/4-08-00-02907/Pregn-4-ene-3,20-dione, 11,21-dihydroxy-, (11β)-/4-Pregnene-11b,21-diol-3,20-dione/11b,21-Dihydroxy-4-pregnene-3,20-dione/(11β)-11,21-Dihydroxypregn-4-ene-3,20-dione/Pregn-4-ene-3,20-dione, 11,21-dihydroxy-, (11-β)- (9CI)/11b,21-Dihydroxyprogesterone/(8S,9S,10R,11S,13S,14S,17S)-11-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-1,2,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthren-3-one/(11b)-11,21-Dihydroxypregn-4-ene-3,20-dione/11b,21-Dihydroxypregn-4-ene-3,20-dione/Pregn-4-ene-3,20-dione, 11-β,21-dihydroxy-/4-08-00-02907 (Beilstein Handbook Reference)/4-Pregnene-11β,21-diol-3,20-dione

IUPAC Name

(8S,9S,10R,11S,13S,14S,17S)-11-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-1,2,6,7,8,9,11,12,14,15,16,17-dodecahydrocyclopenta[a]phenanthren-3-one

Density

1.2±0.1 g/cm3

Solubility

Flash Point

288.0±26.6 °C

Boiling Point

529.2±50.0 °C at 760 mmHg

Melting Point

179-183 °C(lit.)

InChl

InChl Key

OMFXVFTZEKFJBZ-HJTSIMOOSA-N

WGK Germany

RID/ADR

HS Code Reference

2937290000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:50-22-6) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

32068372

Abstract

Immune defense is costly to maintain and deploy, and the optimal investment into immune defense depends on risk of infection. Altitude is a natural environmental factor that is predicted to affect parasite abundance, with lower parasite abundance predicted at higher altitudes due to stronger environmental stressors, which reduce parasite transmission. Using high and low altitude populations of the Turkish blind mole-rat (TBMR) Nannospalax xanthodon, we tested for effects of altitude on constitutive innate immune defense. Field studies were performed with 32 wild animals in 2017 and 2018 from two low- and one high-altitude localities in the Central Taurus Mountains, at respective altitudes of 1010 m, 1115 m, and 2900 m above sea level. We first compared innate standing immune defense as measured by the bacteria-killing ability of blood serum. We then measured corticosterone stress hormone levels, as stressful conditions may affect immune response. Finally, we compared prevalence and intensity of gastrointestinal parasites of field-captured TBMR. We found that the bacteria-killing ability of serum is greater in the mole-rat samples from high altitude. There was no significant difference in stress (corticosterone) levels between altitude categories. Coccidian prevalence and abundance were significantly higher in 2017 than 2018 samples, but there was no significant difference in prevalence, abundance, or intensity between altitudes, or between sexes. Small sample sizes may have reduced power to detect true differences; nevertheless, this study provides support that greater standing innate immunity in high altitude animals may reflect greater investment into constitutive defense.

KEYWORDS

Nannospalax; altitude; ecoimmunology; gastro-intestinal parasites; immune response; stress

Title

Altitudinal Effects on Innate Immune Response of a Subterranean Rodent.

Author

Solak HM1, Yanchukov A1, colak F1, Matur F2, Sozen M1, Ayanoglu İC3, Winternitz JC4.

Publish date

2020 Feb;

PMID

31972205

Abstract

BACKGROUND:
Higher levels of glucocorticoids (GCs), and impaired regulation of the hypothalamic-pituitary-adrenal (HPA) axis may cause or exacerbate the occurrence of metabolic and psychiatric disorders. It has been reported that ginseng saponin extract (GSE) has an inhibitory effect on the hyperactivity of the HPA axis induced by stresses and increased corticosterone level induced by intraperitoneal injection of adrenocorticotrophic hormone (ACTH) in mice. However, the molecular mechanisms by which GSE and its active ginsenosides inhibit corticosterone secretion remain elusive.

MAIN METHODS:
Y1 mouse adrenocortical cells were treated with ACTH for up to 60 min to establish a cell model of corticosterone secretion. After treatment with different concentrations of GSE or ginsenoside monomers for 24 h prior to the addition of ACTH, analyses of cAMP content, PKA activity, and the levels of steroidogenesis regulators, melanocortin-2 receptor (MC2R), and melanocortin-2 receptor accessory protein (MRAP) in ACTH-induced Y1 cells were performed.

RESULTS:
We demonstrated that GSE inhibits ACTH-stimulated corticosterone production in Y1 cells by inhibiting factors critical for steroid synthesis. Ginsenoside Rd, an active ingredient of GSE, inhibits corticosterone secretion in the cells and impedes ACTH-induced corticosterone biosynthesis through down-regulation of proteins in the cAMP/PKA/CREB signaling pathway. In addition, Western blot and qPCR analyses showed that ginsenoside Rd attenuated the induction of MC2R and MRAP by ACTH.

CONCLUSION:
Our findings indicate that ginsenoside Rd inhibits ACTH-induced corticosterone production through blockading the MC2R-cAMP/PKA/CREB pathway in adrenocortical cells. Overall, this mechanism may represent an important therapeutic option for the treatment of stress-related disorders, further supporting the pharmacological benefits of ginseng.

Copyright © 2020 Elsevier Inc. All rights reserved.

KEYWORDS

Adrenocorticotropic hormone (ACTH); Corticosterone secretion; Ginsenoside Rd; Melanocortin-2 receptor (MC2R); cAMP/PKA/CREB signaling

Title

Ginsenoside Rd attenuates ACTH-induced corticosterone secretion by blocking the MC2R-cAMP/PKA/CREB pathway in Y1 mouse adrenocortical cells.

Author

Jin W1, Ma R1, Zhai L1, Xu X1, Lou T1, Huang Q1, Wang J1, Zhao D2, Li X3, Sun L4.

Publish date

2020 Mar 15;

PMID

31937214

Abstract

Life-history theory predicts that, to optimize their fitness, individuals should increase their reproductive effort as their residual reproductive value decreases. Accordingly, several studies have shown that individuals downregulate their glucocorticoid stress response (a proxy of reproductive investment in vertebrates) as they age, and as the subsequent reproductive value decreases. However, and surprisingly, results appear inconsistent, suggesting that the environmental context or the individual state may affect the relationship between age and reproductive effort. Here, we tested for the first time this hypothesis, and more specifically, whether this attenuation of the corticosterone stress response with advancing age depends on the energetic status of individuals. We compared the influence of age on the corticosterone stress response between fasting and non-fasting breeding snow petrels (Pagodroma nivea), an extremely long-lived bird. As expected, we found that the corticosterone stress response was attenuated in old petrels, but only when they were not fasting. Interestingly, this pattern was not apparent in fasting petrels, suggesting that old birds downregulate their corticosterone stress response and increase their parental investment only when they are in good body condition. At the ultimate level, old individuals may maintain a strong corticosterone stress response when fasting because the survival costs of increased stress resistance and parental effort might then outweigh their reproductive benefits.

KEYWORDS

age; corticosterone; parental effort; seabirds; stress

Title

When do older birds better resist stress? A study of the corticosterone stress response in snow petrels.

Author

Angelier F1, Chastel O1, Lendvai AZ2, Parenteau C1, Weimerskirch H1, Wingfield JC3.

Publish date

2020 Jan;1