Corticosterone
(Synonyms: 皮质酮; 17-Deoxycortisol; 11β,21-Dihydroxyprogesterone; Kendall's compound B) 目录号 : GC12327
Corticosterone (17 deoxycortisol) 是一种具有口服活性的糖皮质激素，由肾上腺皮质产生，对调节边缘系统（包括海马、前额叶皮层和杏仁核）的神经元功能具有重要作用。
Cas No.:50-22-6
Sample solution is provided at 25 µL, 10mM.
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Related Biological Data
Effect of compounds 1–17 on corticosterone-treated SH-SY5Y cells.The Cort group was treated with corticosterone (200 μM) for 48 h.The compound groups were treated with 200 μM corticosterone for 24 h, followed by corticosterone and different concentrations (0.1, 1, 10 and 100 μM) of compounds 1–17 for 24 h.
The Cort group was treated with corticosterone (GLPBIO) (200 μM) for 48 h.
J Ethnopharmacol (2022): 115430. PMID: 35659626 IF: 4.3603 -
Related Biological Data
Baicalin Ameliorates CORT-Induced Depressive-Like Behaviors in Mice. A: Sucrose preference test, B: novelty suppressed feeding test, C: forced swimming test, D: tail suspension test, E: elevated plus maze test.
The control group received subcutaneous injections of 0.9% saline only, and the other 4 groups received subcutaneous injections of CORT (Glpbio) (40 mg/kg) in the first 3 weeks.
Chin J Integr Med 29.5 (2023): 405-412. PMID: 36607586 IF: 2.8997 -
Related Biological Data
Effect of OCT Transporters on Cellular Uptake (c) an inhibitor of OCT3, corticosterone
However, corticosterone (Glpbio) (20 μg/mL), an OCT3 inhibitor, only had a significant effect in the accumulation of 1,000 ng/mL fluoxetine.
Current Drug Delivery 19.4 (2022): 508-517. PMID: 34238184 IF: 2.5652 -
Related Biological Data
Baicalin and Lithium enhanced the activity of CORT induced PC-12 cells. (B) Cell survival of PC-12 cells after different concentrations of CORT treatment.
Corticosterone (CORT) was obtained from Glpbio (Montclair, CA,USA).
Biol Pharm Bull (2022): b21-01046. PMID: 35296580 IF: 2.2332 -
Related Biological Data
Effects of prazosin and corticosterone on the brain–plasma ratio in rats. (A) FLT enantiomers; (B) NFLT enantiomers.
Corticosterone was provided by GLPBIO (USA).
Chirality (2023). PMID: 37464916 IF: 1.9999
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| Cell experiment [1]: | |
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Cell lines |
The white preadipocyte cell line 3T3-L1 and the brown preadipocyte cell line T37i |
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Preparation Method |
Three hours before stimulation, the differentiated cells were starved in starvation medium: DMEM (for 3T3-L1) or DMEM/F12 with 20 mM HEPES (for T37i) supplemented with P/S and 0.2% dextran-coated charcoal-treated FBS. Subsequently, the cells were stimulated for 24 hours in starvation medium containing 1 µL/mL ethanol vehicle control, 1 µM corticosterone, 0.2 µM insulin, or 1 µM corticosterone and 0.2 µM insulin. |
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Reaction Conditions |
1 µM for 15min |
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Applications |
Corticosterone treatment altered many aspects of WAT and BAT morphology and function with some clear differences between male and female mice. The visceral depot gWAT had a substantially greater mass in vehicle-treated male mice than in vehicle-treated female mice. This sex-dependent pattern disappeared after corticosterone treatment, as corticosterone-treated male and female mice had a comparable gWAT mass. Two subcutaneous depots, iWAT and aWAT, also gained more mass upon corticosterone treatment, but there was no significant sex difference. Corticosterone treatment noticeably elevated the total WAT mass (the sum of the aforementioned WAT masses) without a significant sex difference. |
| Animal experiment [2]: | |
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Animal models |
Female BALB/c mice |
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Preparation Method |
The mice (three-to-four-week-old) were randomly divided into control group and Corticosterone group. Each mouse in the treatment group was injected with Corticosterone. Corticosterone was dissolved in DMSO to reach a concentration 0.2 mg/µL. The control group was injected with the same volume of DMSO. The treatment procedures were briefly presented as follows: On the first day at 7:00 a.m., mice were injected with 10 IU of PMSG. The control group (n = 40) and the test group (n = 40) were injected with 5 µL of DMSO and 5 µL of Corticosterone (0.2 mg/µL) every 8 hours. |
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Dosage form |
0.2 mg/µL |
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Applications |
Corticosterone group's weight gain of the (1 mg/mouse) was slowed down, the action was slow, and the coat color was dull, compared with the control group. The ovary at each stage was weighed and the organ index was calculated. The results are shown in Figure 1. At 48 h, the gain of body weight in the Corticosterone group was significantly lower than that of the control group. Ovarian weight and ovarian index in the Corticosterone group was significantly lower than that of the control group. At 55 h, the gain of body weight, ovarian weight and ovarian index of the Corticosterone group were significantly lower than those of the control group. |
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References: [1]. Kaikaew K, Steenbergen J, van Dijk T H, et al. Sex difference in corticosterone-induced insulin resistance in mice[J]. Endocrinology, 2019, 160(10): 2367-2387. |
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Corticosterone (17 deoxycortisol) is a glucocorticoid with oral activity and produced by adrenal cortex, which plays an important role in regulating the neuronal function of limbic system (including hippocampus, prefrontal cortex and amygdala). Corticosterone increased Rab mediated AMPAR membrane trafficking through SGK induced phosphorylation of GDI [1].
Corticosterone has been shown to cause hippocampal damage in a number of ways; altering dendritic tree of hippocampal neurons, apoptosis of hippocampal neurons [2]and inhibition of adult neurogenesis in dentate gyrus[3]. Firstly, high concentrations of Corticosterone were required to induce neuronal death in mouse hippocampal neurons, and secondly, glial cells in cultures were refractory to Corticosterone -induced apoptosis. Corticosterone induced apoptosis in primary cultures of hippocampal neurons in a dose dependent manner. Significant apoptosis started to be seen with 50 μM Corticosterone, and the number of apoptotic cells increased with increase in Corticosterone concentration [4].
Corticosterone-treated male mice were more severe whole-body insulin resistance in the, the high blood insulin concentrations upon corticosterone treatment resulted in lower glucose production in male mice but not in female mice. Because GCs stimulate and insulin suppresses hepatic gluconeogenesis, it is hard to separate the contribution of these two factors in the control of EGP. Quinn et al[5] have shown that female mice have a higher hepatic susceptibility to GCs. Thus, more pronounced actions of GCs in female mice might overrule the inhibitory effect of insulin on EGP or, alternatively, the FBG levels of corticosterone-treated mice were at their lowest limit, which requires EGP to prevent symptomatic hypoglycemia. Corticosterone treatment had opposite effects on GCR in male and female mice. GCR tended to increase in female mice but tended to decrease in male mice. These findings confirm that peripheral insulin resistance was more severe in corticosterone-treated males than in corticosterone-treated females because the elevated insulin levels by corticosterone treatment should have increased GCR substantially in both sexes. Altogether, The sex-differential effects of high-dose corticosterone treatment on insulin sensitivity were mainly driven by the more pronounced insulin resistance of peripheral tissues in male mice [6].
References:
[1] Gasser PJ, et al. Corticosterone-sensitive monoamine transport in the rat dorsomedial hypothalamus: potential role for organiccation transporter 3 in stress-induced modulation of monoaminergic neurotransmission. J Neurosci. 2006 Aug 23;26(34):8758-8766.
[2] Liu B, Zhang H, Xu C, et al. Neuroprotective effects of icariin on corticosterone-induced apoptosis in primary cultured rat hippocampal neurons[J]. Brain research, 2011, 1375: 59-67.
[3] Yu I T, Lee S H, Lee Y S, et al. Differential effects of corticosterone and dexamethasone on hippocampal neurogenesis in vitro[J]. Biochemical and biophysical research communications, 2004, 317(2): 484-490.
[4] Latt H M, Matsushita H, Morino M, et al. Oxytocin inhibits corticosterone-induced apoptosis in primary hippocampal neurons[J]. Neuroscience, 2018, 379: 383-389.
[5] Quinn M A, Xu X, Ronfani M, et al. Estrogen deficiency promotes hepatic steatosis via a glucocorticoid receptor-dependent mechanism in mice[J]. Cell reports, 2018, 22(10): 2690-2701.
[6] Wei Y, Li W, Meng X, et al. Corticosterone Injection Impairs Follicular Development, Ovulation and Steroidogenesis Capacity in Mice Ovary[J]. Animals, 2019, 9(12): 1047.
Corticosterone (17 deoxycortisol) 是一种具有口服活性的糖皮质激素，由肾上腺皮质产生，对调节边缘系统（包括海马、前额叶皮层和杏仁核）的神经元功能具有重要作用。皮质酮通过 SGK 诱导的 GDI 磷酸化增加 Rab 介导的 AMPAR 膜运输[1]。
皮质酮已被证明会以多种方式引起海马体损伤；改变海马神经元的树突树，海马神经元细胞凋亡 [2] 并抑制成年齿状回神经发生[3]。首先，需要高浓度的皮质酮来诱导小鼠海马神经元中的神经元死亡，其次，培养物中的神经胶质细胞对皮质酮诱导的细胞凋亡具有抵抗力。皮质酮以剂量依赖性方式诱导海马神经元原代培养物的细胞凋亡。 50 μM 皮质酮开始观察到明显的细胞凋亡，凋亡细胞的数量随着皮质酮浓度的增加而增加[4]。
皮质酮治疗的雄性小鼠全身胰岛素抵抗更严重，皮质酮治疗后的高血液胰岛素浓度导致雄性小鼠的葡萄糖生成降低，但雌性小鼠则没有。因为 GCs 刺激而胰岛素抑制肝糖异生，所以很难区分这两个因素在 EGP 控制中的作用。 Quinn 等人[5] 表明，雌性小鼠对 GC 具有更高的肝脏易感性。因此，GCs 在雌性小鼠中更明显的作用可能会否决胰岛素对 EGP 的抑制作用，或者，皮质酮治疗小鼠的 FBG 水平处于最低限度，这需要 EGP 来预防症状性低血糖。皮质酮治疗对雄性和雌性小鼠的 GCR 有相反的影响。 GCR 在雌性小鼠中趋于增加，但在雄性小鼠中趋于降低。这些发现证实，外周胰岛素抵抗在皮质酮治疗的男性中比在皮质酮治疗的女性中更严重，因为皮质酮治疗升高的胰岛素水平应该在两种性别中都显着增加 GCR。总而言之，高剂量皮质酮治疗对胰岛素敏感性的性别差异影响主要是由雄性小鼠外周组织更明显的胰岛素抵抗驱动的[6]。
| Cas No. | 50-22-6 | SDF | |
| 别名 | 皮质酮; 17-Deoxycortisol; 11β,21-Dihydroxyprogesterone; Kendall's compound B | ||
| 化学名 | (8S,9S,10R,11S,13S,14S,17S)-11-hydroxy-17-(2-hydroxyacetyl)-10,13-dimethyl-6,7,8,9,10,11,12,13,14,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-3(2H)-one | ||
| Canonical SMILES | O[C@@H]1[C@H]([C@](CC2)(C)C3=CC2=O)[C@@H](CC3)[C@H]4[C@]([C@@H](C(CO)=O)CC4)(C)C1 | ||
| 分子式 | C21H30O4 | 分子量 | 346.46 |
| 溶解度 | ≥ 14.5mg/mL in DMSO | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.8863 mL | 14.4317 mL | 28.8634 mL |
| 5 mM | 0.5773 mL | 2.8863 mL | 5.7727 mL |
| 10 mM | 0.2886 mL | 1.4432 mL | 2.8863 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
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2.
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Corticosterone's roles in avian migration: Assessment of three hypotheses
While corticosterone (CORT) is often suggested to be an important hormone regulating processes necessary for avian migration, there has been no systematic assessment of CORT's role in migration. Prior to migration, birds increase fat stores and flight muscle size to prepare for the high energetic costs associated with long-distance flight. After attaining sufficient energetic stores, birds then make the actual decision to depart from their origin site. Once en route birds alternate between periods of flight and stopovers, during which they rest and refuel for their next bouts of endurance flight. Here, we evaluate three non-mutually exclusive hypotheses that have been proposed in the literature for CORT's role in migration. (1) CORT facilitates physiological preparations for migration [e.g. hyperphagia, fattening, and flight muscle hypertrophy]. (2) CORT stimulates departure from origin or stopover sites. (3) CORT supports sustained migratory travel. After examining the literature to test predictions stemming from each of these three hypotheses, we found weak support for a role of CORT in physiological preparation for migration. However, we found moderate support for a role of CORT in stimulating departures, as CORT increases immediately prior to departure and is higher when migratory restlessness is displayed. We also found moderate support for the hypothesis that CORT helps maintain sustained travel, as CORT is generally higher during periods of flight, though few studies have tested this hypothesis. We provide recommendations for future studies that would help to further resolve the role of CORT in migration.
Measuring corticosterone in feathers: Strengths, limitations, and suggestions for the future
The recently introduced technique of measuring corticosterone in feathers currently provides the longest-term measure of corticosterone in birds. This review examines the strengths, weaknesses, and unresolved technical issues of the feather corticosterone technique. Feather corticosterone's major strengths are that it provides: a retrospective assessment of corticosterone physiology, including information from absent (unseen) or dead (e.g. museum specimens) individuals; a long-term measure of corticosterone exposure over the period of feather growth (days-weeks), integrating both baseline and responses to stressors; and flexible, minimally-invasive, sampling. However, researchers considering this technique should be aware of its limitations. Feather corticosterone only reflects hormone exposure during feather growth and, when sampling during molt, corticosterone titers and ecological conditions may not be representative of the majority of the annual cycle. Synchronization of molt is often unknown for a population, requiring assumptions when making inter-individual comparisons. Additionally, unresolved technical issues include: assessing whether corticosterone is the only hormone measured by assays; determining deposition dynamics to fully understand connections between feather and plasma corticosterone titers; studying the longevity and stability of corticosterone in the feather; establishing the impact of feather size and color on corticosterone deposition; and understanding the causes and implications of corticosterone variation along the length of the feather. Notwithstanding the above limitations and technical challenges, determining corticosterone titers in feathers is proving to be a useful technique for exploring some ecological and physiological correlates in individual birds. Given the unique perspective that feather corticosterone offers, we suggest that this measure complement, not replace, plasma measurements.
Effects of corticosterone on BDNF expression and mood behaviours in mice
Stress hormones such as cortisol play a critical role in depressive disorders. Therefore, corticosterone has been used to develop a depression model in animals. Our previous studies found that the precursor of brain-derived neurotrophic factor (proBDNF) and its receptors are upregulated in depression in human and animal models. In the present study, we aimed to examine whether proBDNF and mature BDNF (mBDNF) are altered in the corticosterone-induced depression model in mice. Male and female mice were given corticosterone dissolved in 0.3% hydroxypropyl- 汕-cyclodextrin (汕-CD) or vehicle (汕-CD) in drinking water for 33 days. We have found that corticosterone induced depressive-like behaviours as reflected by increased immobility time in the tail suspension test and decreased grooming time in the splash test. Corticosterone also induced anxiety-like behaviours as represented by decreased entries into the central zone of the open field test and the open arms of the elevated plus maze test. We found that corticosterone administration resulted in differential changes of proBDNF and mature BDNF in different brain regions and peripheral tissues. ProBDNF was increased in the hippocampus and cerebellum, but no change was found in the prefrontal cortex and hypothalamus. Both proBDNF and mBDNF were significantly increased in the pituitary gland. In contrast, proBDNF was significantly decreased in the adrenal gland. There were no significant changes in proBDNF or mBDNF in other peripheral tissues, including the liver and sex organs. We conclude that the stress hormone corticosterone causes depressive behaviours but differentially regulates the processing of proBDNF in mice. ProBDNF may participate in the development of depression behaviours in corticosterone treated animals.
Testicular induced corticosterone synthesis in male rats under fasting stress
Testicular steroidogenesis is depressed by adrenal-secreted corticosterone (CORT) under stress. However, the mechanisms are not well understood. This study investigated the details of testicular steroidogenesis depression during fasting. Blood levels of adrenocorticotropic hormone secreted from the pituitary glands increased, but blood CORT was not changed in rats that fasted for 96 h, in spite of the rats being severely stressed. CORT in fasting adult male rats increased more than three times in the testis, but reduced testicular testosterone (T) and blood T levels to 5% and 2% of the control, respectively, was observed. The contents of T precursor (except PGN) were drastically reduced in the fasted-rat testes. Testicular CORT levels were elevated, but the enzymatic activity of cytochrome P45011汕, which produces CORT, remained unchanged. The enzymatic activities of 3汕-hydroxysteroid dehydrogenase (3汕-HSD), mediating the conversion of pregnenolone to progesterone, decreased in the fasted-rat testes. Thus, fasting suppressed testicular steroidogenesis by affecting the enzyme activity of 3汕-HSD in the testes and drastically reduced T and increased CORT synthesis. It can be considered that T synthesis involved in cell proliferation is suppressed due to lack of energy during fasting. Conversely, 11汕-hydroxylase enzyme activity was induced and CORT synthesis is increased to cope with the fasting stress. Hence, it can be concluded that CORT synthesis in the testes plays a role in the local defense response.
Corticosterone triggers anti-proliferative and apoptotic effects, and downregulates the ACVR1-SMAD1-ID3 cascade in chicken ovarian prehierarchical, but not preovulatory granulosa cells
The coordinated proliferation and apoptosis of granulosa cells plays a critical role in follicular development. To identify the exact mechanisms of how stress-driven glucocorticoid production suppresses reproduction, granulosa cells were isolated from chicken follicles at different developmental stages and then treated with corticosterone. Using CCK-8, EDU and TUNEL assays, we showed that corticosterone could trigger both anti-proliferative and pro-apoptotic effects in granulosa cells from 6 to 8 mm follicles only, while depicting no influence on granulosa cells from any preovulatory follicles. High-throughput transcriptomic analysis identified 1362 transcripts showing differential expression profiles in granulosa cells from 6 to 8 mm follicles after corticosterone treatment. Interestingly, Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that 17 genes were enriched in the TGF-汕 signaling pathway, and 13 showed differential expression patterns consistent with corticosterone-induced effects. The differential expression profiles of these 13 genes were examined by quantitative real-time PCR in cultured chicken ovarian granulosa cells at diverse developmental stages following corticosterone challenge for a short (8 h) or long period (24 h). After 24 h of treatment, INHBB, FST, FMOD, NOG, ACVR1, SMAD1 and ID3 were the genes that responded consistently with corticosterone-induced proliferative and apoptotic events in all granulosa cells detected. However, only ACVR1, SMAD1 and ID3 could initiate coincident expression patterns after being treated for 8 h, suggesting their significance in corticosterone-mediated actions. Collectively, these findings indicate that corticosterone can inhibit proliferation and cause apoptosis in chicken ovarian prehierarchical, but not preovulatory granulosa cells, through impeding ACVR1-SMAD1-ID3 signaling presumptively.