Background:

Hydrocortisone is a steroid hormone or glucocorticoid secreted by the adrenal cortex.

Hydrocortisone (50 nM) shows a dose-dependent down-regulation of GR transcript in hCMEC/D3 cells. Hydrocortisone supplementation of the serum-reduced cell differentiation medium leads to a significant increase in TER across the hCMEC/D3 monolayer[1]. Hydrocortisone-treated Dendritic cells (DCs) show a decreased expression of MHC II molecules, the costimulatory molecule CD86, and the DC-specific marker CD83, as well as a strongly reduced IL-12 secretion. Hydrocortisone-treated DCs inhibit production of IFN-γ but induce an increased release of IL-4 and no change in IL-5[2]. Hydrocortisone reduces postischemic oxidative stress, perfusion pressure, and transudate formation. Hydrocortisone inhibits postischemic shedding of syndecan-1, heparan sulfate, and hyaluronan as is release of histamine from resident mast cells[3].

参考文献:
[1]. F rster C, et al. Differential effects of hydrocortisone and TNFalpha on tight junction proteins in an in vitro model of the human blood-brain barrier. J Physiol. 2008 Apr 1;586(7):1937-49.
[2]. Bellinghausen I, et al. Inhibition of human allergic T-cell responses by IL-10-treated dendritic cells: differences from hydrocortisone-treated dendritic cells. J Allergy Clin Immunol. 2001 Aug;108(2):242-9.
[3]. Chappell D, et al. Hydrocortisone preserves the vascular barrier by protecting the endothelial glycocalyx. Anesthesiology. 2007 Nov;107(5):776-84.