Acceleration of neutrophil precursors’ maturation and immunostimulation of CD3+, CD4+ lymphocytes by stanozolol in mice

Inamdar, Laxmi S.; Jayamma, Y.

doi:10.1016/j.jsbmb.2011.11.008

Cited by 19 publications

(13 citation statements)

References 53 publications

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“…Young women who suffered from polycystic ovarian syndrome have hyperandrogenism and elevated neutrophil counts, and the increase of neutrophils could be overcome via treatment with the antiandrogen, flutamide, suggesting that androgen and AR signaling promote neutrophil development . This suggestion was further validated by another study demonstrating that androgen treatment accelerates neutrophil precursor's maturation in the in vivo mouse system . Collectively, androgen and AR signals play a stimulatory role in neutrophil differentiation from HSCs.…”

Section: Ar Roles In Hscsmentioning

confidence: 68%

Concise Review: Androgen Receptor Differential Roles in Stem/Progenitor Cells Including Prostate, Embryonic, Stromal, and Hematopoietic Lineages

et al. 2014

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Stem/progenitor (S/P) cells are special types of cells that have the ability to generate tissues throughout their entire lifetime and play key roles in the developmental process. Androgen and the androgen receptor (AR) signals are the critical determinants in male gender development, suggesting that androgen and AR signals might modulate the behavior of S/P cells. In this review, we summarize the AR effects on the behavior of S/P cells, including self-renewal, proliferation, apoptosis, and differentiation in normal S/P cells, as well as proliferation, invasion, and self-renewal in prostate cancer S/P cells. AR plays a protective role in the oxidative stress-induced apoptosis in embryonic stem cells. AR inhibits the self-renewal of embryonic stem cells, bone marrow stromal cells, and prostate S/P cells, but promotes their differentiation except for adipogenesis. However, AR promotes the proliferation of hematopoietic S/P cells and stimulates hematopoietic lineage differentiation. In prostate cancer S/P cells, AR suppresses their self-renewal, metastasis, and invasion. Together, AR differentially influences the characteristics of normal S/P cells and prostate cancer S/P cells, and targeting AR might improve S/P cell transplantation therapy, especially in embryonic stem cells and bone marrow stromal cells.

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Section: Ar Roles In Hscsmentioning

confidence: 68%

Concise Review: Androgen Receptor Differential Roles in Stem/Progenitor Cells Including Prostate, Embryonic, Stromal, and Hematopoietic Lineages

et al. 2014

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“…Similarly, androgen-deficient prostate cancer patients and gona-dectomized male mice also display neutropenia, prior to androgen-replacement therapy/DHT treatment ( 48 , 49 ). Further support for androgen-induced granulopoiesis and neutrophil differentiation comes from studies of stanozolol, a testosterone analog, showing an increased prevalence of myelocytes and metamyelocytes as well as accelerated neutrophil maturation in treated female mice ( 50 ). Neutrophilia can also be observed in young women with hyperandrogenism due to polycystic ovarian syndrome ( 47 ).…”

Section: Androgens and Immune Cell Subsetsmentioning

confidence: 99%

Androgen-Induced Immunosuppression

2018

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In addition to determining biological sex, sex hormones are known to influence health and disease via regulation of immune cell activities and modulation of target-organ susceptibility to immune-mediated damage. Systemic autoimmune disorders, such as systemic lupus erythematosus, rheumatoid arthritis, and multiple sclerosis are more prevalent in females, while cancer shows the opposite pattern. Sex hormones have been repeatedly suggested to play a part in these biases. In this review, we will discuss how androgens and the expression of functional androgen receptor affect immune cells and how this may dampen or alter immune response(s) and affect autoimmune disease incidences and progression.

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“…The animals were fed a standard rodent chow diet (Probiotério, Moinho Primor, Brazil) for 8 weeks to evaluate the effects of stanozolol (17β‐hydroxy‐17‐methyl‐5α‐androstano(3,2‐c)pyrazole) (Stanozolol Depot, Landerlan group; 50 mg/mL) on the spontaneous progression of atherosclerosis. The animals were randomly separated into two groups: (a) control group (C; n = 8) in which the animals were fed the normal diet and treated with the vehicle for stanozolol that was saline solution (NaCl, 0.9%); and (b) stanozolol‐treated group (S; n = 8) in which the animals were fed with a normal diet and treated with a high dose of stanozolol (20 mg/kg/wk) .…”

Section: Methodsmentioning

confidence: 99%

“…The evidence shows that stanozolol is capable of increasing the concentrations of low‐density lipoprotein cholesterol (LDL‐C), stimulating the immune response and promoting oxidative stress . All of these processes are crucial for the development of atherosclerosis .…”

Section: Introductionmentioning

confidence: 99%

Stanozolol promotes lipid deposition in the aorta through an imbalance in inflammatory cytokines and oxidative status in LDLr knockout mice fed a normal diet

Andrade

Haguihara

Falsoni

et al. 2018

Basic Clin Pharma Tox

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The aim of the study was to evaluate the effect of an anabolic steroid, stanozolol, in a model of atherosclerosis and to investigate the involvement of the modulation of the inflammatory cytokines and oxidative stress in vascular lipid deposition.Low-density lipid receptor-deficient (LDLr−/−) mice were fed a standard chow diet and were each week injected subcutaneously either saline (control C group) or 20 mg/kg stanozolol (S group). After 8 weeks, the levels of cholesterol, oxidized LDL (OxLDL) and cytokines were measured in plasma, lipid deposition in aorta was evaluated by en face analysis, and thiobarbituric acid-reactive substances and oxidation protein were determined in liver. The S group demonstrated increases in vascular lipid deposition, triglycerides and non-HDL cholesterol levels. Stanozolol increased tumour necrosis factor alpha (TNF-α) and decreased interleukin-10 as well as increased the TNF-α/IL-10 ratio. Furthermore, oxidative stress was observed in the S group, as indicated by an increase in the plasma OxLDL, as well as by lipid peroxidation and oxidation of proteins in the liver. Chronic treatment with stanozolol promoted lipid deposition in the LDLr −/− mice that could be attributed to a modification of the circulating cytokine levels and systemic oxidative stress. Our results suggest that the anabolic steroid stanozolol in the absence of functional LDL receptors by increasing systemic inflammation and oxidative stress may increase the risk of development and progression of atherosclerosis.

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Acceleration of neutrophil precursors’ maturation and immunostimulation of CD3+, CD4+ lymphocytes by stanozolol in mice

Cited by 19 publications

References 53 publications

Concise Review: Androgen Receptor Differential Roles in Stem/Progenitor Cells Including Prostate, Embryonic, Stromal, and Hematopoietic Lineages

Concise Review: Androgen Receptor Differential Roles in Stem/Progenitor Cells Including Prostate, Embryonic, Stromal, and Hematopoietic Lineages

Androgen-Induced Immunosuppression

Stanozolol promotes lipid deposition in the aorta through an imbalance in inflammatory cytokines and oxidative status in LDLr knockout mice fed a normal diet

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