在外周血单核细胞 (PBMC) 中，可的松 (2.8-28,000 nM) 剂量依赖性地减少皮质醇诱导的细胞凋亡 [1]。

在兔子中，可的松（2 mg/kg；每隔一天肌肉注射一次，持续两个月）可降低结核菌素反应和 BCG（结核分枝杆菌疫苗株）病变 [2]。

糖皮质激素（GC）被认为通过诱导胸腺细胞和成熟外周血淋巴细胞凋亡来调节免疫细胞系统。在这里，我们报道了皮质醇在有丝分裂原活化的外周血单核细胞（PBMC）中诱导的细胞凋亡被皮质醇的氧化代谢产物可的松抑制。PBMC中的细胞凋亡通过细胞死亡ELISA程序进行定量，该程序可以特异性检测片段化的DNA。皮质醇在刀豆球蛋白A刺激的PBMC中以大于10ng/ml（28nM）的浓度诱导PBMC凋亡，并且皮质醇在1-10000ng/ml（2.8-28000nM）浓度范围内剂量依赖性地抑制这种凋亡。泼尼松，一种合成的氧化GC，也以剂量依赖的方式抑制皮质醇的凋亡诱导作用。在来自16名健康受试者的PBMC中一致观察到可的松对皮质醇诱导的细胞凋亡的抑制。类固醇对[3H]地塞米松与PBMC结合的抑制活性的检查表明，可的松可以与细胞GC受体（GC Rs）结合，但可的松与GC Rs的亲和力为皮质醇的1/30或更低。这一结果提出了可的松在皮质醇介导的活化人PBMC细胞凋亡调控中的可能作用。可的松对皮质醇诱导的细胞凋亡的抵消作用可能部分通过GC受体（GC Rs）的干预发生，但也可能是由于与细胞GC Rs介导的途径不同的未知途径[1]。

Animal/Disease Models: Male New Zealand white rabbits (2.1-2.4 kg) were injected with BCG six days after the first dose [2]
Doses: 2 mg/kg
Route of Administration: intramuscularinjection every other day for 2 months
Experimental Results: BCG lesions and tuberculosis bacteria were diminished factor reaction. diminished the number of infiltrating mononuclear cells (MN), the number of caseous necrosis and ulcers, and the percentage of β-galactosidase-positive NMs.

Absorption, Distribution and Excretion
Corticosteroids are eliminated predominantly in the urine.
Data regarding the clearance of cortisone acetate is not readily available.

Protein Binding
Corticosteroids are generally bound to corticosteroid binding globulin and serum albumin in plasma.

[1]. Cortisone counteracts apoptosis-inducing effect of cortisol in human peripheral-blood mononuclear cells. Int Immunopharmacol. 2001 Nov;1(12):2109-15.

[2]. The effect of cortisone on the accumulation, activation, and necrosis of macrophages in tuberculous lesions. Inflammation. 1978 Jun;3(2):159-76.

[3]. In Vivo Antifungal Activity of Monolaurin against Candida albicans Biofilms. Biol Pharm Bull. 2018;41(8):1299-1302.

[4]. In vivo effects of cortisone on the B cell line in chickens. J Immunol. 1975 Nov;115(5):1370-4.

Cortisone acetate is a corticosteroid hormone.
Cortisone acetate was first isolate in 1935 and became more widely researched in 1949. Since then, glucocorticoids such as cortisone acetate have been used to treat a number of inflammatory conditions such as endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, respiratory, hematologic, neoplastic, edematous, and gastrointestinal diseases and disorders. Cortisone acetate was granted FDA approval on 13 June 1950.
Cortisone Acetate is the acetate salt form of cortisone, a synthetic or semisynthetic analog of the naturally occurring cortisone hormone produced by the adrenal glands with anti-inflammatory and immunomodulating properties. Cortisone acetate diffuses through the cell membrane and binds to nuclear glucocorticoid receptors. The receptor-ligand complex binds to promotor regions of certain genes and initiates RNA transcription. This results in an induction of synthesis of certain anti-inflammatory proteins while inhibiting the synthesis of certain inflammatory mediators.
A naturally occurring glucocorticoid that has been used in replacement therapy for ADRENAL INSUFFICIENCY and as an anti-inflammatory agent. Cortisone itself is inactive; it is converted in the liver to the active metabolite HYDROCORTISONE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p726)
See also: Cortisone (has active moiety) ... View More ...

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Drug Indication
Cortisone acetate is indicated to treat a wide variety of endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, respiratory, hematologic, neoplastic, edematous, and gastrointestinal diseases and disorders.

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Mechanism of Action
The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days. Glucocorticoids inhibit neutrophil apoptosis and demargination; they inhibit phospholipase A2, which decreases the formation of arachidonic acid derivatives; they inhibit NF-Kappa B and other inflammatory transcription factors; they promote anti-inflammatory genes like interleukin-10. Lower doses of corticosteroids provide an anti-inflammatory effect, while higher doses are immunosuppressive. High doses of glucocorticoids for an extended period bind to the mineralocorticoid receptor, raising sodium levels and decreasing potassium levels.

C23H30O6

402.48

402.204

C, 68.64; H, 7.51; O, 23.85

50-04-4

Cortisone;53-06-5

5745

Typically exists as white to off-white solids at room temperature

1.3±0.1 g/cm3

577.3±50.0 °C at 760 mmHg

237-240 °C(lit.)

197.3±23.6 °C

0.0±3.6 mmHg at 25°C

1.566

2.53

97.74

1

6

4

29

827

6

O([H])[C@]1(C(C([H])([H])OC(C([H])([H])[H])=O)=O)C([H])([H])C([H])([H])[C@@]2([H])[C@]3([H])C([H])([H])C([H])([H])C4=C([H])C(C([H])([H])C([H])([H])[C@]4(C([H])([H])[H])[C@@]3([H])C(C([H])([H])[C@@]21C([H])([H])[H])=O)=O

ITRJWOMZKQRYTA-RFZYENFJSA-N

InChI=1S/C23H30O6/c1-13(24)29-12-19(27)23(28)9-7-17-16-5-4-14-10-15(25)6-8-21(14,2)20(16)18(26)11-22(17,23)3/h10,16-17,20,28H,4-9,11-12H2,1-3H3/t16-,17-,20+,21-,22-,23-/m0/s1

2-((8S,9S,10R,13S,14S,17R)-17-hydroxy-10,13-dimethyl-3,11-dioxo-2,3,6,7,8,9,10,11,12,13,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl)-2-oxoethyl acetate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

配方 1 中的溶解度: ≥ 0.5 mg/mL (1.24 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 5.0 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 0.5 mg/mL (1.24 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 5.0 mg/mL 澄清 DMSO 储备液加入 900 μL 20% SBE-β-CD 生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 0.5 mg/mL (1.24 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 5.0 mg/mL 澄清 DMSO 储备液加入到 900 μL 玉米油中并混合均匀。

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配方 4 中的溶解度: 25 mg/mL (62.11 mM) in 0.1% Tween-80 in PBS (这些助溶剂从左到右依次添加，逐一添加), 悬浊液; 超声助溶。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。