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Endocrine

pp 1–7 | Cite as

Capsaicin inhibits lipopolysaccharide-induced adrenal steroidogenesis by raising intracellular calcium levels

  • Leonardo G. B. Ferreira
  • Jessika P. Prevatto
  • Hercules R. Freitas
  • Ricardo A. M. Reis
  • Patrícia M. R. Silva
  • Marco A. Martins
  • Robson X. Faria
  • Vinicius F. CarvalhoEmail author
Original Article
  • 5 Downloads

Abstract

Introduction

Glucocorticoid release by adrenals has been described as significant to survive sepsis. The activation of transient receptor potential vanilloid type 1 (TRPV1) inhibited ACTH-induced glucocorticoid release by adrenal glands in vitro.

Objective

The aim of this study was to investigate if capsaicin, an activator of TRPV1, would prevent LPS-induced glucocorticoid production by adrenals.

Methods

Male Swiss-Webster mice were treated with capsaicin intraperitoneally (0.2 or 2 mg/kg) 30 min before LPS injection. All analyses were performed 2 h after the LPS stimulation, including plasma corticosterone and peritoneal IL-1β and TNF-α levels. Furthermore, murine adrenocortical Y1 cells were used to assess the effects of capsaicin on LPS-induced corticosterone production in vitro.

Results

Capsaicin (2 mg/kg, i.p.) significantly reduced plasma corticosterone levels and adrenal hypertrophy induced by LPS without alter the levels of pro-steroidogenic cytokines IL-1β and TNF-α in peritoneal cavity of mice, while the dose of 0.2 mg/kg of capsaicin did not interfere with adrenal steroidogenesis, attested by RIA and ELISA, respectively. Y1 cells express TRPV1, measured by immunofluorescence and western blot, and capsaicin decreased LPS-induced corticosterone production by these cells in vitro. Capsaicin also induces calcium mobilization in Y1 cells in vitro.

Conclusions

These findings suggest that capsaicin inhibits corticosterone production induced by LPS by acting directly on adrenal cells producing glucocorticoids, in a mechanism probably associated with induction of a cytoplasmic calcium increase in these cells.

Keywords

Calcium Capsaicin Glucocorticoid LPS Steroidogenesis TRPV1 

Notes

Acknowledgments

This work was supported by grants from the Conselho Nacional de Desenvolvimento Científico and Tecnológico (CNPq), Instituto Nacional de Ciência e Tecnologia em Neuroimunomodulação (INCT-NIM), Instituto Nacional de Ciência e Tecnologia em Neurociência Translacional (INNT-INCT), Fundação Carlos Chagas de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ), Programa de Auxílio à Pesquisa (PAPESVI/FIOCRUZ), and Ministério da Saúde, Brazil.

Compliance with ethical standards

Conflict of interest

The authors declare that they have no conflict of interest.

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Copyright information

© Springer Science+Business Media, LLC, part of Springer Nature 2019

Authors and Affiliations

  • Leonardo G. B. Ferreira
    • 1
  • Jessika P. Prevatto
    • 1
  • Hercules R. Freitas
    • 2
  • Ricardo A. M. Reis
    • 2
  • Patrícia M. R. Silva
    • 1
  • Marco A. Martins
    • 1
  • Robson X. Faria
    • 3
  • Vinicius F. Carvalho
    • 1
    • 4
    Email author
  1. 1.Laboratório de Inflamação, Instituto Oswaldo CruzFundação Oswaldo CruzManguinhosBrazil
  2. 2.Laboratório de Neuroquímica, Instituto de Biofísica Carlos Chagas FilhoUniversidade Federal do Rio de JaneiroIlha do FundãoBrazil
  3. 3.Laboratório de Toxoplasmose e Outras ProtozoosesInstituto Oswaldo Cruz, Fundação Oswaldo CruzManguinhosBrazil
  4. 4.Instituto Nacional de Ciência e Tecnologia em Neuroimunomodulação (INCT-NIM)ManguinhosBrazil

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