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Evaluation of Brown Micro-Algae Synergies With Low Dose γ-Radiation Against Chronic Hepatitis Induced by D-Galactosamine in Rats

INTRODUCTION: Hepatic inflammation is considered key driver of hepatic tissue impairment.We aimed to explore the interaction of Halamphora coffeaeformis (Amph.) with low dose ionizing γ radiation (γR) exposure against D-galactosamine (D-GaIN)-induced chronic hepatitis in Albino rats. METHODS: Chroni...

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Autores principales: Elsaman, Salma, Elsonbaty, Sawsan M., Moawed, Fatma S. M., Hegazy, Marwa G. A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: SAGE Publications 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10107994/
https://www.ncbi.nlm.nih.gov/pubmed/37077716
http://dx.doi.org/10.1177/15593258231169405
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author Elsaman, Salma
Elsonbaty, Sawsan M.
Moawed, Fatma S. M.
Hegazy, Marwa G. A.
author_facet Elsaman, Salma
Elsonbaty, Sawsan M.
Moawed, Fatma S. M.
Hegazy, Marwa G. A.
author_sort Elsaman, Salma
collection PubMed
description INTRODUCTION: Hepatic inflammation is considered key driver of hepatic tissue impairment.We aimed to explore the interaction of Halamphora coffeaeformis (Amph.) with low dose ionizing γ radiation (γR) exposure against D-galactosamine (D-GaIN)-induced chronic hepatitis in Albino rats. METHODS: Chronic hepatitis was induced with single dose of D-GalN (400 mg/kg BW i.p.). Rats received 400 mg Amph/kg BW daily by gastric gavage concomitant with .25 Gy γ-R. Liver oxidative stress and inflammatory status were assessed. Gene expression levels of signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NFKB) were estimated by q-PCR. D-Galactosamine injection significantly encouraged hepatic oxidative damage and inflammatory disturbance accompanied with improved intercellular adhesion molecule-1 level (ICAM-1). RESULTS: messenger RNA gene expression levels of STAT3 and NF-kB were expressively higher in D-GaIN-treated animals. Histopathological examination supported results. Interestingly, Amph treatment with γ-radiation (γ-R) subjection displayed significant improvement of oxidative and inflammatory status along with controlled signaling molecular factors which was supported by amended histological structure of induced liver hepatitis. CONCLUSION: Results conclude the efficacious control of liver hepatitis progression by dual collaboration of Amph. with low dose γ-R via control of vital growth signaling factors linked with inflammation thru anti-inflammation, antioxidative and anti-proliferative activities.
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spelling pubmed-101079942023-04-18 Evaluation of Brown Micro-Algae Synergies With Low Dose γ-Radiation Against Chronic Hepatitis Induced by D-Galactosamine in Rats Elsaman, Salma Elsonbaty, Sawsan M. Moawed, Fatma S. M. Hegazy, Marwa G. A. Dose Response Original Article INTRODUCTION: Hepatic inflammation is considered key driver of hepatic tissue impairment.We aimed to explore the interaction of Halamphora coffeaeformis (Amph.) with low dose ionizing γ radiation (γR) exposure against D-galactosamine (D-GaIN)-induced chronic hepatitis in Albino rats. METHODS: Chronic hepatitis was induced with single dose of D-GalN (400 mg/kg BW i.p.). Rats received 400 mg Amph/kg BW daily by gastric gavage concomitant with .25 Gy γ-R. Liver oxidative stress and inflammatory status were assessed. Gene expression levels of signal transducer and activator of transcription 3 (STAT3) and nuclear factor kappa B (NFKB) were estimated by q-PCR. D-Galactosamine injection significantly encouraged hepatic oxidative damage and inflammatory disturbance accompanied with improved intercellular adhesion molecule-1 level (ICAM-1). RESULTS: messenger RNA gene expression levels of STAT3 and NF-kB were expressively higher in D-GaIN-treated animals. Histopathological examination supported results. Interestingly, Amph treatment with γ-radiation (γ-R) subjection displayed significant improvement of oxidative and inflammatory status along with controlled signaling molecular factors which was supported by amended histological structure of induced liver hepatitis. CONCLUSION: Results conclude the efficacious control of liver hepatitis progression by dual collaboration of Amph. with low dose γ-R via control of vital growth signaling factors linked with inflammation thru anti-inflammation, antioxidative and anti-proliferative activities. SAGE Publications 2023-04-11 /pmc/articles/PMC10107994/ /pubmed/37077716 http://dx.doi.org/10.1177/15593258231169405 Text en © The Author(s) 2023 https://creativecommons.org/licenses/by-nc/4.0/This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).
spellingShingle Original Article
Elsaman, Salma
Elsonbaty, Sawsan M.
Moawed, Fatma S. M.
Hegazy, Marwa G. A.
Evaluation of Brown Micro-Algae Synergies With Low Dose γ-Radiation Against Chronic Hepatitis Induced by D-Galactosamine in Rats
title Evaluation of Brown Micro-Algae Synergies With Low Dose γ-Radiation Against Chronic Hepatitis Induced by D-Galactosamine in Rats
title_full Evaluation of Brown Micro-Algae Synergies With Low Dose γ-Radiation Against Chronic Hepatitis Induced by D-Galactosamine in Rats
title_fullStr Evaluation of Brown Micro-Algae Synergies With Low Dose γ-Radiation Against Chronic Hepatitis Induced by D-Galactosamine in Rats
title_full_unstemmed Evaluation of Brown Micro-Algae Synergies With Low Dose γ-Radiation Against Chronic Hepatitis Induced by D-Galactosamine in Rats
title_short Evaluation of Brown Micro-Algae Synergies With Low Dose γ-Radiation Against Chronic Hepatitis Induced by D-Galactosamine in Rats
title_sort evaluation of brown micro-algae synergies with low dose γ-radiation against chronic hepatitis induced by d-galactosamine in rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10107994/
https://www.ncbi.nlm.nih.gov/pubmed/37077716
http://dx.doi.org/10.1177/15593258231169405
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