Adrenocorticotropic hormone

Adrenocorticotropic hormone (ACTH; Adrenocorticotrophic hormone) is a polypeptide tropic hormone produced by the anterior pituitary gland. Adrenocorticotropic hormone stimulates cortisol secretion from the adrenal cortex via the hypothalamic-pituitary-adrenal (HPA) axis. Adrenocorticotropic hormone regulates cortisol and androgen production. Adrenocorticotropic hormone can promote the development of spermatogenesis. Adrenocorticotropic hormone can relieve acute inflammation in gout models by inhibiting the polarization of macrophages to M1 type, inhibiting ROS and proinflammatory factor production and protecting mitochondrial function. Adrenocorticotropic hormone can be used for the researches of inflammation, endocrinology, metabolic disease, such as gout and nephrotic syndrome^[1][2][3][4]. In Vitro:Adrenocorticotropic hormone (100 nM, 5weeks) induces clusters development of spermatogenesis isolated from mouse seminiferous tubules and significantly increases the proportion of pre-meiotic cells (CDH-1, VASA, MC2R-positive) and the expression of PLZF, VASA, MC2R, THY-1 genes^[2].
Adrenocorticotropic hormone (100 nM, 5weeks) significantly increases the proportion and gene expression of meiotic marker BOULE-positive cells in cells isolated from mouse seminiferous tubules and has no significant effect on the proportion of meiotic marker CREM-positive cells, increases the proportion of post-meiotic marker ACROSIN-positive cells but decreases its gene expression, and has no effect on the expression of SCP3 and PROTAMINE^[2].
Adrenocorticotropic hormone (1.25×10^-4-2.5×10^-4 U/ml, 48 h) inhibits phagocytic function in MSU-stimulated THP-1-induced macrophages, promotes the polarization of MSU-stimulated macrophages to M2 type, downregulates the secretion of M1-type proinflammatory factors IL-1β, IL-6, and TNF-α, inhibit ROS production and reduces the opening of mitochondrial permeability transition pores (mPTP) to protect mitochondrial function^[3].
Adrenocorticotropic hormone (1.25×10^-4 U/ml, 48 h) regulates the transcription of inflammation-related genes by upregulating genes such as NR1H2, IL-37, and FccRIIIA, and downregulating genes such as NLRP3, MC2R, and MC3R in THP-1-induced macrophages^[3].
In Vivo:Adrenocorticotropic hormone (0.25-2.5 U/mL, s.c., 30 minutes after MSU intra-articular injection) significantly alleviates joint swelling, reduces inflammatory cell infiltration in joint tissues, and has no significant effect on serum cortisol levels in gout mice models^[3].