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The anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters

Brain inflammation and apoptosis play crucial roles in the pathogenesis of various neurodevelopmental disorders. Probiotics have been shown to confer protection against many stresses, including apoptosis and inflammation, by modulating the gut function. The short‐chain fatty acid, propionic acid (PP...

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Autores principales: Ben Bacha, Abir, Al‐Orf, Norah, Alonazi, Mona, Bhat, Ramesa Shafi, El‐Ansary, Afaf
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8441441/
https://www.ncbi.nlm.nih.gov/pubmed/34531999
http://dx.doi.org/10.1002/fsn3.2435
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author Ben Bacha, Abir
Al‐Orf, Norah
Alonazi, Mona
Bhat, Ramesa Shafi
El‐Ansary, Afaf
author_facet Ben Bacha, Abir
Al‐Orf, Norah
Alonazi, Mona
Bhat, Ramesa Shafi
El‐Ansary, Afaf
author_sort Ben Bacha, Abir
collection PubMed
description Brain inflammation and apoptosis play crucial roles in the pathogenesis of various neurodevelopmental disorders. Probiotics have been shown to confer protection against many stresses, including apoptosis and inflammation, by modulating the gut function. The short‐chain fatty acid, propionic acid (PPA), plays an important intermediate of cellular metabolism. Although PPA exhibits numerous beneficial biological effects, its accumulation is neurotoxic. This study focused on the therapeutic potency of probiotics against PPA‐induced apoptosis and neuroinflammation in hamsters. Five groups of male golden Syrian hamsters were treated as follows: Group I as control; Group II as PPA‐treated with three doses of 250 mg PPA/kg/day; Group III as clindamycin‐treated with a single dose of 30 mg clindamycin/kg; Group IV as PPA–probiotic; and Group V as clindamycin–probiotic were two therapeutic groups which were treated with the same doses of PPA and clindamycin, respectively, followed by treatment with 0.2 g kg(‐1) d(−1) of probiotic (Protexin(R), Probiotics International Limited) for three weeks. Proapoptotic markers, such as caspases 3 and 7; neuroinflammation markers, such as interleukins 1β and 8; and heat shock protein 70 were measured in the brain. Significant increase of all measured markers (p ˂ .001) was observed in PPA and clindamycin‐treated hamsters compared with controls. Probiotics significantly reduced the damages and ameliorated all the test markers in both therapeutic groups compared with the control. Our results confirmed that probiotics can be utilized as a feasible strategy for managing apoptotic and inflammation‐related stresses in brain disorders by retaining the gut function.
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spelling pubmed-84414412021-09-15 The anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters Ben Bacha, Abir Al‐Orf, Norah Alonazi, Mona Bhat, Ramesa Shafi El‐Ansary, Afaf Food Sci Nutr Original Research Brain inflammation and apoptosis play crucial roles in the pathogenesis of various neurodevelopmental disorders. Probiotics have been shown to confer protection against many stresses, including apoptosis and inflammation, by modulating the gut function. The short‐chain fatty acid, propionic acid (PPA), plays an important intermediate of cellular metabolism. Although PPA exhibits numerous beneficial biological effects, its accumulation is neurotoxic. This study focused on the therapeutic potency of probiotics against PPA‐induced apoptosis and neuroinflammation in hamsters. Five groups of male golden Syrian hamsters were treated as follows: Group I as control; Group II as PPA‐treated with three doses of 250 mg PPA/kg/day; Group III as clindamycin‐treated with a single dose of 30 mg clindamycin/kg; Group IV as PPA–probiotic; and Group V as clindamycin–probiotic were two therapeutic groups which were treated with the same doses of PPA and clindamycin, respectively, followed by treatment with 0.2 g kg(‐1) d(−1) of probiotic (Protexin(R), Probiotics International Limited) for three weeks. Proapoptotic markers, such as caspases 3 and 7; neuroinflammation markers, such as interleukins 1β and 8; and heat shock protein 70 were measured in the brain. Significant increase of all measured markers (p ˂ .001) was observed in PPA and clindamycin‐treated hamsters compared with controls. Probiotics significantly reduced the damages and ameliorated all the test markers in both therapeutic groups compared with the control. Our results confirmed that probiotics can be utilized as a feasible strategy for managing apoptotic and inflammation‐related stresses in brain disorders by retaining the gut function. John Wiley and Sons Inc. 2021-07-13 /pmc/articles/PMC8441441/ /pubmed/34531999 http://dx.doi.org/10.1002/fsn3.2435 Text en © 2021 The Authors. Food Science & Nutrition published by Wiley Periodicals LLC. https://creativecommons.org/licenses/by/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Ben Bacha, Abir
Al‐Orf, Norah
Alonazi, Mona
Bhat, Ramesa Shafi
El‐Ansary, Afaf
The anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters
title The anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters
title_full The anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters
title_fullStr The anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters
title_full_unstemmed The anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters
title_short The anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters
title_sort anti‐inflammatory and antiapoptotic effects of probiotic on induced neurotoxicity in juvenile hamsters
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8441441/
https://www.ncbi.nlm.nih.gov/pubmed/34531999
http://dx.doi.org/10.1002/fsn3.2435
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