Antiproliferative activity of the ellagic acid-derived gut microbiota isourolithin A and comparison with its urolithin A isomer: the role of cell metabolism

2015 ◽  
Vol 56 (2) ◽  
pp. 831-841 ◽  
Author(s):  
Antonio González-Sarrías ◽  
María Ángeles Núñez-Sánchez ◽  
Rocío García-Villalba ◽  
Francisco A. Tomás-Barberán ◽  
Juan Carlos Espín
Keyword(s):  
Gut Microbiota ◽  
Antiproliferative Activity ◽  
Ellagic Acid ◽  
Cell Metabolism ◽  
Urolithin A

scholarly journals Gut Microbiota Conversion of Dietary Ellagic Acid into Bioactive Phytoceutical Urolithin A Inhibits Heme Peroxidases

PLoS ONE ◽  
2016 ◽  
Vol 11 (6) ◽  
pp. e0156811 ◽  
Author(s):  
Piu Saha ◽  
Beng San Yeoh ◽  
Rajbir Singh ◽  
Bhargavi Chandrasekar ◽  
Praveen Kumar Vemula ◽  
...  
Keyword(s):  
Gut Microbiota ◽  
Ellagic Acid ◽  
Urolithin A ◽  
Heme Peroxidases

scholarly journals Immunomodulatory Role of Urolithin A on Metabolic Diseases

Biomedicines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 192
Author(s):  
Ashley Mulcahy Toney ◽  
Darius Fox ◽  
Virginia Chaidez ◽  
Amanda E. Ramer-Tait ◽  
Soonkyu Chung
Keyword(s):  
Ellagic Acid ◽  
Dietary Intervention ◽  
Metabolic Diseases ◽  
Therapeutic Potential ◽  
Alcoholic Fatty Liver ◽  
Urolithin A ◽  
Anti Inflammatory ◽  
The Brain

Urolithin A (UroA) is a gut metabolite produced from ellagic acid-containing foods such as pomegranates, berries, and walnuts. UroA is of growing interest due to its therapeutic potential for various metabolic diseases based on immunomodulatory properties. Recent advances in UroA research suggest that UroA administration attenuates inflammation in various tissues, including the brain, adipose, heart, and liver tissues, leading to the potential delay or prevention of the onset of Alzheimer’s disease, type 2 diabetes mellitus, and non-alcoholic fatty liver disease. In this review, we focus on recent updates of the anti-inflammatory function of UroA and summarize the potential mechanisms by which UroA may help attenuate the onset of diseases in a tissue-specific manner. Therefore, this review aims to shed new insights into UroA as a potent anti-inflammatory molecule to prevent immunometabolic diseases, either by dietary intervention with ellagic acid-rich food or by UroA administration as a new pharmaceutical drug.

scholarly journals Gut bacterial metabolite Urolithin A (UA) mitigates Ca2+ entry in T cells by regulating miR-10a-5p

2018 ◽  
Author(s):  
Shaqiu Zhang ◽  
Tamer Al-Maghout ◽  
Hang Cao ◽  
Lisann Pelzl ◽  
Madhuri S Salker ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
T Cells ◽  
T Cell ◽  
Gut Microbiota ◽  
Ellagic Acid ◽  
T Cell Proliferation ◽  
Protein Levels ◽  
Urolithin A ◽  
Dose Dependent Fashion ◽  
Anti Oxidant

ABSTRACTThe gut microbiota influences several biological functions including immune response. Inflammatory bowel disease is favourably influenced by consumption of several dietary natural plant products such as pomegranate, walnuts and berries containing polyphenolic compounds such as ellagitannins and ellagic acid. The gut microbiota metabolises ellagic acid leading to formation of bioactive urolithins A, B, C and D. Urolithin A (UA) is the most active and effective gut metabolite and acts as a potent anti-inflammatory and anti-oxidant agent. However, how gut metabolite UA affects the function of immune cells remained incompletely understood. T cell proliferation is stimulated by store operated Ca2+ entry (SOCE) resulting from stimulation of Orai1 by STIM1/STIM2. We show here that treatment of murine CD4+ T cells with UA (10 µM, 3 days) significantly blunted SOCE in CD4+ T cells, an effect paralleled by significant downregulation of Orai1 and STIM1/2 transcript levels and protein abundance. UA treatment further increased miR-10a-5p abundance in CD4+ T cells in a dose dependent fashion. Overexpression of miR-10a-5p significantly decreased STIM1/2 and Orai1 mRNA and protein levels as well as SOCE in CD4+ T cells. UA further decreased CD4+ T cell proliferation. Thus, bacterial metabolite UA up-regulates miR-10a-5p thus interfering with Orai1/STIM1/STIM2 expression, store operated Ca2+ entry and proliferation of murine CD4+ T cells.

The ellagic acid-derived gut microbiota metabolite, urolithin A, potentiates the anticancer effects of 5-fluorouracil chemotherapy on human colon cancer cells

2015 ◽  
Vol 6 (5) ◽  
pp. 1460-1469 ◽  
Author(s):  
Antonio González-Sarrías ◽  
Joao Tomé-Carneiro ◽  
Andrea Bellesia ◽  
Francisco A. Tomás-Barberán ◽  
Juan Carlos Espín
Keyword(s):  
Colon Cancer ◽  
Gut Microbiota ◽  
Cancer Cells ◽  
Ellagic Acid ◽  
Human Colon ◽  
Colon Cancer Cells ◽  
Human Colon Cancer ◽  
Anticancer Effects ◽  
Urolithin A ◽  
Human Colon Cancer Cells

The ellagic acid-derived gut microbiota metabolite, urolithin A, at concentrations achievable in the human colorectum, enhances the anticancer effects of 5-FU-chemotherapy on three different colon cancer cells.

scholarly journals Urolithin A and B Alter Cellular Metabolism and Induce Metabolites Associated with Apoptosis in Leukemic Cells

2021 ◽  
Vol 22 (11) ◽  
pp. 5465
Author(s):  
Abdulaziz Musa Alzahrani ◽  
Mohammed Razeeth Shait Mohammed ◽  
Raed Ahmed Alghamdi ◽  
Abrar Ahmad ◽  
Mazin A. Zamzami ◽  
...  
Keyword(s):  
Cell Lines ◽  
Ellagic Acid ◽  
Cell Metabolism ◽  
Leukemic Cell ◽  
Glutamine Metabolism ◽  
Leukemic Cells ◽  
Leukemic Cell Lines ◽  
Urolithin A ◽  
One Carbon Metabolism ◽  
Urolithin B

Leukemia is persistently a significant cause of illness and mortality worldwide. Urolithins, metabolites of ellagic acid and ellagitannins produced by gut microbiota, showed better bioactive compounds liable for the health benefits exerted by ellagic acid and ellagitannins containing pomegranate and walnuts. Here, we assessed the potential antileukemic activities of both urolithin A and urolithin B. Results showed that both urolithin A and B significantly inhibited the proliferation of leukemic cell lines Jurkat and K562, among which urolithin A showed the more prominent antiproliferative capability. Further, urolithin treatment alters leukemic cell metabolism, as evidenced by increased metabolic rate and notable changes in glutamine metabolism, one-carbon metabolism, and lipid metabolism. Next, we evidenced that both urolithins equally promoted apoptosis in leukemic cell lines. Based on these observations, we concluded that both urolithin A and B alter leukemic cell metabolome, resulting in a halt of proliferation, followed by apoptosis. The data can be used for designing new combinational therapies to eradicate leukemic cells.

Gut Microbiota and Antipsychotics Induced Metabolic Alteration

2019 ◽  
pp. 131-143
Author(s):  
Dong-Yu Kan ◽  
Su-Juan Li ◽  
Chen-Chen Liu ◽  
Ren-Rong Wu
Keyword(s):  
Gut Microbiota ◽  
Body Weight Gain ◽  
Neuropsychiatric Disorders ◽  
Elevated Risk ◽  
Metabolic Disturbance ◽  
Metabolic Dysfunction ◽  
Sequencing Technology ◽  
Severe Mental Disorder ◽  
Metabolic Alteration

Schizophrenia is a chronic and severe mental disorder with antipsychotics as primary medications, but the antipsychotic-induced metabolic side effects may contribute to the elevated risk of overall morbidity and mortality in patients with psych-iatric diseases. With the development in sequencing technology and bioinformatics, dysbiosis has been shown to contribute to body weight gain and metabolic dysfunction. However, the role of gut microbiota in the antipsychotic-induced metabolic alteration remains unknown. In this paper, we reviewed the recent studies of the gut microbiota with psychiatric disorders and antipsychotic-induced metabolic dysfunction. Patients with neuropsychiatric disorders may have a different composi-tion of gut microbiota compared with healthy controls. In addition, it seems that the use of antipsychotics is concurrently associated with both altered composition of gut microbiota and metabolic disturbance. Further study is needed to address the role of gut microbiota in the development of neuropsychiatric disorders and antipsychotic-induced metabolic disturbance, to develop novel therapeutics for both neuropsychiatric disorders and metabolic dysfunction.

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