17β-estradiol replacement therapy induces enos, nnos and estrogen receptor β in hypophysectomized rats with inflamed footpads

C. Vera-Arzave, J. Pacheco-Yepez, C. M. Mejía-Barradas, L. M. Cárdenas-Jaramillo, R. Campos-Rodríguez, E. Abarca-Rojano

Research output: Contribution to journalArticle

Abstract

Nitric oxide (NO) plays a key role in inflammation. It is partly produced by three forms of NOS: eNOS of inflammatory cells, nNOS of neural cells and iNOS (inducible isoform). Estrogens can cause an anti-inflammatory effect, although it is not yet clear through which NOS isoforms. The aim of this study was to evaluate the role of the different NOS isoforms, as well as estrogen receptors (ERs) α and β, on the anti-inflammatory effects of estrogens. To avoid the influence of endogenous glucocorticoids or sexual hormones, male rats were hypophysectomized. Animals were segregated into two control groups (no-treatment control group and SHAM-operated animals) and three hypophysectomized groups (no-hormonal treatment, with estradiol-17β, or with testosterone replacement treatment). Freund’s complete adjuvant (1 mg) was administered to the footpad of all animals. Measurements were made based on footpad inflammation (with a plethysmometer) such as eNOS, nNOS, iNOS and ER α and β protein expression (by immunohistochemistry principle/method) on days 1, 7 and 14. Only estradiol decreased inflammation, accompanied by increased levels of eNOS and nNOS and differential expression of ERs α and β in the inflammatory infiltrate. The higher levels of estradiol-induced eNOS and nNOS ocurred perhaps through the activation of ER β.

Original languageEnglish
Pages (from-to)1395-1403
Number of pages9
JournalJournal of Biological Regulators and Homeostatic Agents
Volume33
Issue number5
StatePublished - 1 Sep 2019

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Estrogen Receptors
Estradiol
Protein Isoforms
Inflammation
Estrogens
Anti-Inflammatory Agents
Control Groups
Freund's Adjuvant
Glucocorticoids
Testosterone
Nitric Oxide
Therapeutics
Immunohistochemistry
Hormones
estrophilin
salicylhydroxamic acid

Keywords

  • As estrogen receptors α and β
  • ENOS
  • Estradiol
  • Hypothalamic-pituitary-adrenal axis
  • Inflammation
  • INOS
  • NNOS

Cite this

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title = "17β-estradiol replacement therapy induces enos, nnos and estrogen receptor β in hypophysectomized rats with inflamed footpads",
abstract = "Nitric oxide (NO) plays a key role in inflammation. It is partly produced by three forms of NOS: eNOS of inflammatory cells, nNOS of neural cells and iNOS (inducible isoform). Estrogens can cause an anti-inflammatory effect, although it is not yet clear through which NOS isoforms. The aim of this study was to evaluate the role of the different NOS isoforms, as well as estrogen receptors (ERs) α and β, on the anti-inflammatory effects of estrogens. To avoid the influence of endogenous glucocorticoids or sexual hormones, male rats were hypophysectomized. Animals were segregated into two control groups (no-treatment control group and SHAM-operated animals) and three hypophysectomized groups (no-hormonal treatment, with estradiol-17β, or with testosterone replacement treatment). Freund’s complete adjuvant (1 mg) was administered to the footpad of all animals. Measurements were made based on footpad inflammation (with a plethysmometer) such as eNOS, nNOS, iNOS and ER α and β protein expression (by immunohistochemistry principle/method) on days 1, 7 and 14. Only estradiol decreased inflammation, accompanied by increased levels of eNOS and nNOS and differential expression of ERs α and β in the inflammatory infiltrate. The higher levels of estradiol-induced eNOS and nNOS ocurred perhaps through the activation of ER β.",
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T1 - 17β-estradiol replacement therapy induces enos, nnos and estrogen receptor β in hypophysectomized rats with inflamed footpads

AU - Vera-Arzave, C.

AU - Pacheco-Yepez, J.

AU - Mejía-Barradas, C. M.

AU - Cárdenas-Jaramillo, L. M.

AU - Campos-Rodríguez, R.

AU - Abarca-Rojano, E.

PY - 2019/9/1

Y1 - 2019/9/1

N2 - Nitric oxide (NO) plays a key role in inflammation. It is partly produced by three forms of NOS: eNOS of inflammatory cells, nNOS of neural cells and iNOS (inducible isoform). Estrogens can cause an anti-inflammatory effect, although it is not yet clear through which NOS isoforms. The aim of this study was to evaluate the role of the different NOS isoforms, as well as estrogen receptors (ERs) α and β, on the anti-inflammatory effects of estrogens. To avoid the influence of endogenous glucocorticoids or sexual hormones, male rats were hypophysectomized. Animals were segregated into two control groups (no-treatment control group and SHAM-operated animals) and three hypophysectomized groups (no-hormonal treatment, with estradiol-17β, or with testosterone replacement treatment). Freund’s complete adjuvant (1 mg) was administered to the footpad of all animals. Measurements were made based on footpad inflammation (with a plethysmometer) such as eNOS, nNOS, iNOS and ER α and β protein expression (by immunohistochemistry principle/method) on days 1, 7 and 14. Only estradiol decreased inflammation, accompanied by increased levels of eNOS and nNOS and differential expression of ERs α and β in the inflammatory infiltrate. The higher levels of estradiol-induced eNOS and nNOS ocurred perhaps through the activation of ER β.

AB - Nitric oxide (NO) plays a key role in inflammation. It is partly produced by three forms of NOS: eNOS of inflammatory cells, nNOS of neural cells and iNOS (inducible isoform). Estrogens can cause an anti-inflammatory effect, although it is not yet clear through which NOS isoforms. The aim of this study was to evaluate the role of the different NOS isoforms, as well as estrogen receptors (ERs) α and β, on the anti-inflammatory effects of estrogens. To avoid the influence of endogenous glucocorticoids or sexual hormones, male rats were hypophysectomized. Animals were segregated into two control groups (no-treatment control group and SHAM-operated animals) and three hypophysectomized groups (no-hormonal treatment, with estradiol-17β, or with testosterone replacement treatment). Freund’s complete adjuvant (1 mg) was administered to the footpad of all animals. Measurements were made based on footpad inflammation (with a plethysmometer) such as eNOS, nNOS, iNOS and ER α and β protein expression (by immunohistochemistry principle/method) on days 1, 7 and 14. Only estradiol decreased inflammation, accompanied by increased levels of eNOS and nNOS and differential expression of ERs α and β in the inflammatory infiltrate. The higher levels of estradiol-induced eNOS and nNOS ocurred perhaps through the activation of ER β.

KW - As estrogen receptors α and β

KW - ENOS

KW - Estradiol

KW - Hypothalamic-pituitary-adrenal axis

KW - Inflammation

KW - INOS

KW - NNOS

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VL - 33

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