Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice

Context: Compounds to treat hypothyroidism in the absence of cardiac side effects are urgently required. In this regard, γ-aminobutyric acid (GABA) has gained interest due to its anti-anxiolytic, antihypertensive and antioxidant properties, and reported benefits to the thyroid system. Objective: We...

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Main Authors: Haoyue Yang, Ronge Xing, Song Liu, Huahua Yu, Pengcheng Li
Format: Article
Language:English
Published: Taylor & Francis Group 2019-01-01
Series:Pharmaceutical Biology
Subjects:
Online Access:http://dx.doi.org/10.1080/13880209.2018.1563621
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author Haoyue Yang
Ronge Xing
Song Liu
Huahua Yu
Pengcheng Li
author_facet Haoyue Yang
Ronge Xing
Song Liu
Huahua Yu
Pengcheng Li
author_sort Haoyue Yang
collection DOAJ
description Context: Compounds to treat hypothyroidism in the absence of cardiac side effects are urgently required. In this regard, γ-aminobutyric acid (GABA) has gained interest due to its anti-anxiolytic, antihypertensive and antioxidant properties, and reported benefits to the thyroid system. Objective: We investigated the ability of GABA to ameliorate fluoride-induced thyroid injury in mice, and investigated the mechanism(s) associated with GABA-induced protection. Materials and methods: Adult male Kumning mice (N = 90) were exposed to NaF (50 mg/kg) for 30 days as a model of hypothyroidism. To evaluate the effects of GABA administration, fluoride-exposed mice received either thyroid tablets, or low (25 mg/kg), medium (50 mg/kg) or high (75 mg/kg) concentrations of pure GABA orally for 14 days groups (N = 10 each). The effects of low (50 mg/kg); medium (75 mg/kg) and high (100 mg/kg) concentrations of laboratory-separated GABA were assessed for comparison. Effects on thyroid hormone production, oxidative stress, thyroid function-associated genes, and side-effects during therapy were measured. Results: GABA supplementation in fluoride-exposed mice significantly increased the expression of thyroid TG, TPO, and NIS (P < 0.05), significantly improved the thyroid redox state (P < 0.05), modulated the expression of thyroid function-associated genes, conferred liver metabolic protection, and prevented changes to myocardial morphology, thus reducing side effects. Both pure and laboratory-separated GABA displayed comparative protective effects. Discussion and conclusion: Our findings support the assertion that GABA exerts therapeutic potential in hypothyroidism. The design and use of human GABA trials to improve therapeutic outcomes in hypothyroidism are now warranted.
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spelling doaj.art-c1570dc39df54bf294eb4b304d5a81322022-12-21T23:37:57ZengTaylor & Francis GroupPharmaceutical Biology1388-02091744-51162019-01-01571283610.1080/13880209.2018.15636211563621Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming miceHaoyue Yang0Ronge Xing1Song Liu2Huahua Yu3Pengcheng Li4Chinese Academy of SciencesChinese Academy of SciencesChinese Academy of SciencesChinese Academy of SciencesChinese Academy of SciencesContext: Compounds to treat hypothyroidism in the absence of cardiac side effects are urgently required. In this regard, γ-aminobutyric acid (GABA) has gained interest due to its anti-anxiolytic, antihypertensive and antioxidant properties, and reported benefits to the thyroid system. Objective: We investigated the ability of GABA to ameliorate fluoride-induced thyroid injury in mice, and investigated the mechanism(s) associated with GABA-induced protection. Materials and methods: Adult male Kumning mice (N = 90) were exposed to NaF (50 mg/kg) for 30 days as a model of hypothyroidism. To evaluate the effects of GABA administration, fluoride-exposed mice received either thyroid tablets, or low (25 mg/kg), medium (50 mg/kg) or high (75 mg/kg) concentrations of pure GABA orally for 14 days groups (N = 10 each). The effects of low (50 mg/kg); medium (75 mg/kg) and high (100 mg/kg) concentrations of laboratory-separated GABA were assessed for comparison. Effects on thyroid hormone production, oxidative stress, thyroid function-associated genes, and side-effects during therapy were measured. Results: GABA supplementation in fluoride-exposed mice significantly increased the expression of thyroid TG, TPO, and NIS (P < 0.05), significantly improved the thyroid redox state (P < 0.05), modulated the expression of thyroid function-associated genes, conferred liver metabolic protection, and prevented changes to myocardial morphology, thus reducing side effects. Both pure and laboratory-separated GABA displayed comparative protective effects. Discussion and conclusion: Our findings support the assertion that GABA exerts therapeutic potential in hypothyroidism. The design and use of human GABA trials to improve therapeutic outcomes in hypothyroidism are now warranted.http://dx.doi.org/10.1080/13880209.2018.1563621gabathyroid hormone synthesismyocardial preservationanti-hypothyroidism
spellingShingle Haoyue Yang
Ronge Xing
Song Liu
Huahua Yu
Pengcheng Li
Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice
Pharmaceutical Biology
gaba
thyroid hormone synthesis
myocardial preservation
anti-hypothyroidism
title Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice
title_full Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice
title_fullStr Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice
title_full_unstemmed Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice
title_short Analysis of the protective effects of γ-aminobutyric acid during fluoride-induced hypothyroidism in male Kunming mice
title_sort analysis of the protective effects of γ aminobutyric acid during fluoride induced hypothyroidism in male kunming mice
topic gaba
thyroid hormone synthesis
myocardial preservation
anti-hypothyroidism
url http://dx.doi.org/10.1080/13880209.2018.1563621
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AT songliu analysisoftheprotectiveeffectsofgaminobutyricacidduringfluorideinducedhypothyroidisminmalekunmingmice
AT huahuayu analysisoftheprotectiveeffectsofgaminobutyricacidduringfluorideinducedhypothyroidisminmalekunmingmice
AT pengchengli analysisoftheprotectiveeffectsofgaminobutyricacidduringfluorideinducedhypothyroidisminmalekunmingmice