11-deoxy Corticosterone is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as an aldosterone precursor[1]. 11-deoxy Corticosterone is converted to aldosterone by 11β-hydroxylase, which adds a hydroxyl group at the 11th position[2]. Aldosterone is a hormone that regulates electrolyte balance and blood pressure by promoting sodium retention and potassium excretion[3]. 11-deoxy Corticosterone is usually used in the research of hypertension, inflammation, and metabolic disorders[4][5].
In vitro, 11-deoxy Corticosterone (10nM; 3h) significantly decreased glucose uptake in rainbow trout hepatocytes (RTH-149) and reduced apparent permeability in gill epithelial cells (RTgill-W1) after 3 hours of treatment[6].
In vivo, 11-deoxy Corticosterone (50mg/pellet; s.c.) every 21 days for 8 weeks increased cardiac fibrosis and inflammation in wild-type CBA/CaJ mice[7].
References:
[1] Silvestre JS, Robert V, Heymes C, et al. Myocardial production of aldosterone and corticosterone in the rat. Physiological regulation. J Biol Chem. 1998;273(9):4883-4891.
[2] Gao X, Yamazaki Y, Tezuka Y, et al. Pathology of Aldosterone Biosynthesis and its Action. Tohoku J Exp Med. 2021;254(1):1-15.
[3] Otsuka H, Abe M, Kobayashi H. The Effect of Aldosterone on Cardiorenal and Metabolic Systems. Int J Mol Sci. 2023;24(6):5370.
[4] Asla Q, Sardà H, Lerma E, et al. 11-Deoxycorticosterone Producing Adrenal Hyperplasia as a Very Unusual Cause of Endocrine Hypertension: Case Report and Systematic Review of the Literature. Front Endocrinol (Lausanne). 2022;13:846865.
[5] Sturm A, Bury N, Dengreville L, et al. 11-deoxycorticosterone is a potent agonist of the rainbow trout (Oncorhynchus mykiss) mineralocorticoid receptor. Endocrinology. 2005;146(1):47-55.
[6] Zuloaga R, Molina A, Valdés JA. In vitro effects of 11-deoxycorticosterone on hepatocytes and gill epithelial cells of rainbow trout (Oncorhynchus mykiss). Gen Comp Endocrinol. 2025;371:114776.
[7] Fletcher EK, Morgan J, Kennaway DR, et al. Deoxycorticosterone/Salt-Mediated Cardiac Inflammation and Fibrosis Are Dependent on Functional CLOCK Signaling in Male Mice. Endocrinology. 2017;158(9):2906-2917.
11-deoxy Corticosterone是一种由肾上腺产生的类固醇激素,具有盐皮质激素活性,并作为醛固酮的前体[1]。11-deoxy Corticosterone通过11β-羟化酶在第11位添加一个羟基转化为醛固酮[2]。醛固酮是一种通过促进钠潴留和钾排泄来调控电解质平衡和血压的激素[3]。11-deoxy Corticosterone通常用于研究高血压、炎症和代谢紊乱[4][5]。
在体外实验中,11-deoxy Corticosterone(10nM;3小时)显著降低了虹鳟鱼肝细胞(RTH-149)中的葡萄糖摄取,并减少了鳃上皮细胞(RTgill-W1)的表观通透性[6]。
在体内实验中,11-deoxy Corticosterone(50mg/pellet皮下注射;每21天一次)在8周内增加了野生型CBA/CaJ小鼠的心脏纤维化和炎症[7]。
















