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Miodesin(TM) Positively Modulates the Immune Response in Endometrial and Vaginal Cells

Endometriosis presents high prevalence and its physiopathology involves hyperactivation of endometrial and vaginal cells, especially by bacteria. The disease has no cure and therapies aiming to inhibit its development are highly desirable. Therefore, this study investigated whether Miodesin(TM) (10...

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Autores principales: Oliveira, Carlos Rocha, Polonini, Hudson, Marcucci, Maria Cristina, Vieira, Rodolfo P.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837934/
https://www.ncbi.nlm.nih.gov/pubmed/35164046
http://dx.doi.org/10.3390/molecules27030782
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author Oliveira, Carlos Rocha
Polonini, Hudson
Marcucci, Maria Cristina
Vieira, Rodolfo P.
author_facet Oliveira, Carlos Rocha
Polonini, Hudson
Marcucci, Maria Cristina
Vieira, Rodolfo P.
author_sort Oliveira, Carlos Rocha
collection PubMed
description Endometriosis presents high prevalence and its physiopathology involves hyperactivation of endometrial and vaginal cells, especially by bacteria. The disease has no cure and therapies aiming to inhibit its development are highly desirable. Therefore, this study investigated whether Miodesin(TM) (10 µg/mL = IC(80); 200 µg/mL = IC(50)), a natural compound constituted by Uncaria tomentosa, Endopleura uchi, and astaxanthin, could exert anti-inflammatory and anti-proliferative effects against Lipopolysaccharides (LPS) stimulation in endometrial and Candida albicans vaginal cell lines. VK2 E6/E7 (vaginal) and KLE (epithelial) cell lines were stimulated with Candida albicans (1 × 10(7) to 5 × 10(7)/mL) and LPS (1 μg/mL), respectively. Miodesin(TM) inhibited mRNA expression for Nuclear factor kappa B (NF-κB), ciclo-oxigenase 1 (COX-1), and phospholipase A2 (PLA2), beyond the C–C motif chemokine ligand 2 (CCL2), CCL3, and CCL5 in VK2 E6/E7 cells (p < 0.05). In addition, the inhibitory effects of both doses of Miodesin(TM) (10 µg/mL and 200 µg/mL) resulted in reduced secretion of interleukin-1β (IL-1β), IL-6, IL-8, tumor necrosis factor α (TNF-α) (24 h, 48 h, and 72 h) and CCL2, CCL3, and CLL5 (p < 0.05) by VK2 E6/E7 cells. In the same way, COX-1 Miodesin(TM) inhibited LPS-induced hyperactivation of KLE cells, as demonstrated by reduced secretion of IL-1β, IL-6, IL-8, TNF-α (24 h, 48 h, and 72 h) and CCL2, CCL3, and CLL5 (p < 0.05). Furthermore, Miodesin(TM) also inhibited mRNA expression and secretion of matrix metalloproteinase-2 (MMP-2), MMP-9, and vascular endothelial growth factor (VEGF), which are key regulators of invasion of endometrial cells. Thus, the study concludes that Miodesin(TM) presents beneficial effects in the context of endometriosis, positively affecting the inflammatory and proliferative response.
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spelling pubmed-88379342022-02-13 Miodesin(TM) Positively Modulates the Immune Response in Endometrial and Vaginal Cells Oliveira, Carlos Rocha Polonini, Hudson Marcucci, Maria Cristina Vieira, Rodolfo P. Molecules Article Endometriosis presents high prevalence and its physiopathology involves hyperactivation of endometrial and vaginal cells, especially by bacteria. The disease has no cure and therapies aiming to inhibit its development are highly desirable. Therefore, this study investigated whether Miodesin(TM) (10 µg/mL = IC(80); 200 µg/mL = IC(50)), a natural compound constituted by Uncaria tomentosa, Endopleura uchi, and astaxanthin, could exert anti-inflammatory and anti-proliferative effects against Lipopolysaccharides (LPS) stimulation in endometrial and Candida albicans vaginal cell lines. VK2 E6/E7 (vaginal) and KLE (epithelial) cell lines were stimulated with Candida albicans (1 × 10(7) to 5 × 10(7)/mL) and LPS (1 μg/mL), respectively. Miodesin(TM) inhibited mRNA expression for Nuclear factor kappa B (NF-κB), ciclo-oxigenase 1 (COX-1), and phospholipase A2 (PLA2), beyond the C–C motif chemokine ligand 2 (CCL2), CCL3, and CCL5 in VK2 E6/E7 cells (p < 0.05). In addition, the inhibitory effects of both doses of Miodesin(TM) (10 µg/mL and 200 µg/mL) resulted in reduced secretion of interleukin-1β (IL-1β), IL-6, IL-8, tumor necrosis factor α (TNF-α) (24 h, 48 h, and 72 h) and CCL2, CCL3, and CLL5 (p < 0.05) by VK2 E6/E7 cells. In the same way, COX-1 Miodesin(TM) inhibited LPS-induced hyperactivation of KLE cells, as demonstrated by reduced secretion of IL-1β, IL-6, IL-8, TNF-α (24 h, 48 h, and 72 h) and CCL2, CCL3, and CLL5 (p < 0.05). Furthermore, Miodesin(TM) also inhibited mRNA expression and secretion of matrix metalloproteinase-2 (MMP-2), MMP-9, and vascular endothelial growth factor (VEGF), which are key regulators of invasion of endometrial cells. Thus, the study concludes that Miodesin(TM) presents beneficial effects in the context of endometriosis, positively affecting the inflammatory and proliferative response. MDPI 2022-01-25 /pmc/articles/PMC8837934/ /pubmed/35164046 http://dx.doi.org/10.3390/molecules27030782 Text en © 2022 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
Oliveira, Carlos Rocha
Polonini, Hudson
Marcucci, Maria Cristina
Vieira, Rodolfo P.
Miodesin(TM) Positively Modulates the Immune Response in Endometrial and Vaginal Cells
title Miodesin(TM) Positively Modulates the Immune Response in Endometrial and Vaginal Cells
title_full Miodesin(TM) Positively Modulates the Immune Response in Endometrial and Vaginal Cells
title_fullStr Miodesin(TM) Positively Modulates the Immune Response in Endometrial and Vaginal Cells
title_full_unstemmed Miodesin(TM) Positively Modulates the Immune Response in Endometrial and Vaginal Cells
title_short Miodesin(TM) Positively Modulates the Immune Response in Endometrial and Vaginal Cells
title_sort miodesin(tm) positively modulates the immune response in endometrial and vaginal cells
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8837934/
https://www.ncbi.nlm.nih.gov/pubmed/35164046
http://dx.doi.org/10.3390/molecules27030782
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