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Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor

Around the world, polycystic ovary syndrome (PCOS) is a complex endocrine-metabolic condition that typically affects 6–20% of females. Our study’s major goal was to examine how chlorogenic acid (CGA) affected mice with endocrine and metabolic problems brought on by letrozole-induced PCOS. Group I se...

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Autores principales: Shah, Mohd Zahoor ul Haq, Shrivastava, Vinoy Kumar, Sofi, Shazia, Jamous, Yahya F., Khan, Mohd Faiyaz, Alkholifi, Faisal K., Ahmad, Wasim, Mir, Manzoor Ahmad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10045653/
https://www.ncbi.nlm.nih.gov/pubmed/36979879
http://dx.doi.org/10.3390/biomedicines11030900
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author Shah, Mohd Zahoor ul Haq
Shrivastava, Vinoy Kumar
Sofi, Shazia
Jamous, Yahya F.
Khan, Mohd Faiyaz
Alkholifi, Faisal K.
Ahmad, Wasim
Mir, Manzoor Ahmad
author_facet Shah, Mohd Zahoor ul Haq
Shrivastava, Vinoy Kumar
Sofi, Shazia
Jamous, Yahya F.
Khan, Mohd Faiyaz
Alkholifi, Faisal K.
Ahmad, Wasim
Mir, Manzoor Ahmad
author_sort Shah, Mohd Zahoor ul Haq
collection PubMed
description Around the world, polycystic ovary syndrome (PCOS) is a complex endocrine-metabolic condition that typically affects 6–20% of females. Our study’s major goal was to examine how chlorogenic acid (CGA) affected mice with endocrine and metabolic problems brought on by letrozole-induced PCOS. Group I served as the control for 81 days; Group II was given Letrozole (LETZ) orally at a dose of 6 mg/kg bw for 21 days to induce PCOS; Group III was given LETZ (6 mg/kg) for 21 days, followed by treatment with CGA (50 mg/kg bw daily) for 60 days. The study indicated that LETZ-treated mice displayed symptoms of PCOS, such as dyslipidemia, hyperinsulinemia, elevated testosterone, increases in inflammatory markers and malonaldehyde, and a decline in antioxidants (Ar, lhr, fshr, and esr2) in the ovaries. These alterations were affected when the mice were given CGA and were associated with reduced levels of adiponectin. Adiponectin showed interactions with hub genes, namely MLX interacting protein like (MLXIPL), peroxisome proliferator-activated receptor gamma Coactivator 1- alpha (PPARGC1), peroxisome proliferator-activated receptor gamma (Pparg), and adiponectin receptor 1 (Adipor1). Lastly, the gene ontology of adiponectin revealed that adiponectin was highly involved in biological processes. The findings from our research suggest that adiponectin has direct impacts on metabolic and endocrine facets of PCOS.
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spelling pubmed-100456532023-03-29 Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor Shah, Mohd Zahoor ul Haq Shrivastava, Vinoy Kumar Sofi, Shazia Jamous, Yahya F. Khan, Mohd Faiyaz Alkholifi, Faisal K. Ahmad, Wasim Mir, Manzoor Ahmad Biomedicines Article Around the world, polycystic ovary syndrome (PCOS) is a complex endocrine-metabolic condition that typically affects 6–20% of females. Our study’s major goal was to examine how chlorogenic acid (CGA) affected mice with endocrine and metabolic problems brought on by letrozole-induced PCOS. Group I served as the control for 81 days; Group II was given Letrozole (LETZ) orally at a dose of 6 mg/kg bw for 21 days to induce PCOS; Group III was given LETZ (6 mg/kg) for 21 days, followed by treatment with CGA (50 mg/kg bw daily) for 60 days. The study indicated that LETZ-treated mice displayed symptoms of PCOS, such as dyslipidemia, hyperinsulinemia, elevated testosterone, increases in inflammatory markers and malonaldehyde, and a decline in antioxidants (Ar, lhr, fshr, and esr2) in the ovaries. These alterations were affected when the mice were given CGA and were associated with reduced levels of adiponectin. Adiponectin showed interactions with hub genes, namely MLX interacting protein like (MLXIPL), peroxisome proliferator-activated receptor gamma Coactivator 1- alpha (PPARGC1), peroxisome proliferator-activated receptor gamma (Pparg), and adiponectin receptor 1 (Adipor1). Lastly, the gene ontology of adiponectin revealed that adiponectin was highly involved in biological processes. The findings from our research suggest that adiponectin has direct impacts on metabolic and endocrine facets of PCOS. MDPI 2023-03-14 /pmc/articles/PMC10045653/ /pubmed/36979879 http://dx.doi.org/10.3390/biomedicines11030900 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Shah, Mohd Zahoor ul Haq
Shrivastava, Vinoy Kumar
Sofi, Shazia
Jamous, Yahya F.
Khan, Mohd Faiyaz
Alkholifi, Faisal K.
Ahmad, Wasim
Mir, Manzoor Ahmad
Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor
title Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor
title_full Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor
title_fullStr Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor
title_full_unstemmed Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor
title_short Chlorogenic Acid Restores Ovarian Functions in Mice with Letrozole-Induced Polycystic Ovarian Syndrome Via Modulation of Adiponectin Receptor
title_sort chlorogenic acid restores ovarian functions in mice with letrozole-induced polycystic ovarian syndrome via modulation of adiponectin receptor
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10045653/
https://www.ncbi.nlm.nih.gov/pubmed/36979879
http://dx.doi.org/10.3390/biomedicines11030900
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