Cargando…

Preventive role of cinnamaldehyde against tenuazonic acid- and Freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model

INTRODUCTION: This study was designed to assess the protective role of cinnamaldehyde (Cin) against the synergistic effect of tenuazonic acid (TeA) and Freund’s adjuvant on different organs of Swiss albino mice. METHODS: TeA was administered singly and in combination with Freund’s adjuvant intra-per...

Descripción completa

Detalles Bibliográficos
Autores principales: Kumari, Ankita, Singh, Karuna
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10325827/
https://www.ncbi.nlm.nih.gov/pubmed/37426034
http://dx.doi.org/10.3389/fmicb.2023.1159881
_version_ 1785069299055984640
author Kumari, Ankita
Singh, Karuna
author_facet Kumari, Ankita
Singh, Karuna
author_sort Kumari, Ankita
collection PubMed
description INTRODUCTION: This study was designed to assess the protective role of cinnamaldehyde (Cin) against the synergistic effect of tenuazonic acid (TeA) and Freund’s adjuvant on different organs of Swiss albino mice. METHODS: TeA was administered singly and in combination with Freund’s adjuvant intra-peritoneally. The mice were divided into control (vehicle treated), mycotoxicosis-induced (MI) groups, and treatment groups. The route of administration of TeA was intra-peritoneal. The treatment group (FAICT) received Cin orally as a protective agent against TeA-induced mycotoxicosis. The effects on performance, differential leukocyte counts (DLC), and pathological measurements in eight organs (liver, lungs, kidney, spleen, stomach, heart, brain, and testis) were taken into consideration. RESULTS: The body weight and feed consumption decreased significantly in the MI groups, which were reversed in the FAICT group. The necropsy observations revealed an increase in the relative organ-to-body weight percentage in the MI groups, which was restored to normal in the FAICT group. Freund’s adjuvant enhanced the effects of TeA on DLC. The antioxidant enzymes SOD and CAT decreased, while MDA increased in the MI groups. Caspase-3 activity was reduced in all organs and remained stable in the treatment group. TeA elevated the ALT concentration in the liver and kidneys and the AST in the liver, kidney, heart, and brain tissues. The oxidative stress induced by TeA in the MI groups was ameliorated in the treatment group. Histopathological observations consisted of NASH, pulmonary oedema and fibrosis, renal crystals and inflammation, splenic hyperplasia, gastric ulceration and cyst, cerebral axonopathy, testicular hyperplasia, and vacuolation in the MI groups. However, no such pathology was recorded in the treatment group. DISCUSSIONS: Thus, it can be concluded that the toxicity of TeA was found to be enhanced when combined with Freund’s adjuvant. However, Cin exhibited promising protective effects against TeA + Freund’s adjuvant toxicity and reverted the pathological alterations caused by them. Additionally, this study emphasizes Freund’s adjuvant’s ability to increase mycotoxicity rather than just acting as an immunopotentiator.
format Online
Article
Text
id pubmed-10325827
institution National Center for Biotechnology Information
language English
publishDate 2023
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-103258272023-07-07 Preventive role of cinnamaldehyde against tenuazonic acid- and Freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model Kumari, Ankita Singh, Karuna Front Microbiol Microbiology INTRODUCTION: This study was designed to assess the protective role of cinnamaldehyde (Cin) against the synergistic effect of tenuazonic acid (TeA) and Freund’s adjuvant on different organs of Swiss albino mice. METHODS: TeA was administered singly and in combination with Freund’s adjuvant intra-peritoneally. The mice were divided into control (vehicle treated), mycotoxicosis-induced (MI) groups, and treatment groups. The route of administration of TeA was intra-peritoneal. The treatment group (FAICT) received Cin orally as a protective agent against TeA-induced mycotoxicosis. The effects on performance, differential leukocyte counts (DLC), and pathological measurements in eight organs (liver, lungs, kidney, spleen, stomach, heart, brain, and testis) were taken into consideration. RESULTS: The body weight and feed consumption decreased significantly in the MI groups, which were reversed in the FAICT group. The necropsy observations revealed an increase in the relative organ-to-body weight percentage in the MI groups, which was restored to normal in the FAICT group. Freund’s adjuvant enhanced the effects of TeA on DLC. The antioxidant enzymes SOD and CAT decreased, while MDA increased in the MI groups. Caspase-3 activity was reduced in all organs and remained stable in the treatment group. TeA elevated the ALT concentration in the liver and kidneys and the AST in the liver, kidney, heart, and brain tissues. The oxidative stress induced by TeA in the MI groups was ameliorated in the treatment group. Histopathological observations consisted of NASH, pulmonary oedema and fibrosis, renal crystals and inflammation, splenic hyperplasia, gastric ulceration and cyst, cerebral axonopathy, testicular hyperplasia, and vacuolation in the MI groups. However, no such pathology was recorded in the treatment group. DISCUSSIONS: Thus, it can be concluded that the toxicity of TeA was found to be enhanced when combined with Freund’s adjuvant. However, Cin exhibited promising protective effects against TeA + Freund’s adjuvant toxicity and reverted the pathological alterations caused by them. Additionally, this study emphasizes Freund’s adjuvant’s ability to increase mycotoxicity rather than just acting as an immunopotentiator. Frontiers Media S.A. 2023-06-22 /pmc/articles/PMC10325827/ /pubmed/37426034 http://dx.doi.org/10.3389/fmicb.2023.1159881 Text en Copyright © 2023 Kumari and Singh. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Microbiology
Kumari, Ankita
Singh, Karuna
Preventive role of cinnamaldehyde against tenuazonic acid- and Freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model
title Preventive role of cinnamaldehyde against tenuazonic acid- and Freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model
title_full Preventive role of cinnamaldehyde against tenuazonic acid- and Freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model
title_fullStr Preventive role of cinnamaldehyde against tenuazonic acid- and Freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model
title_full_unstemmed Preventive role of cinnamaldehyde against tenuazonic acid- and Freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model
title_short Preventive role of cinnamaldehyde against tenuazonic acid- and Freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model
title_sort preventive role of cinnamaldehyde against tenuazonic acid- and freund’s adjuvant-induced histopathological and biochemical alterations in the mouse model
topic Microbiology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10325827/
https://www.ncbi.nlm.nih.gov/pubmed/37426034
http://dx.doi.org/10.3389/fmicb.2023.1159881
work_keys_str_mv AT kumariankita preventiveroleofcinnamaldehydeagainsttenuazonicacidandfreundsadjuvantinducedhistopathologicalandbiochemicalalterationsinthemousemodel
AT singhkaruna preventiveroleofcinnamaldehydeagainsttenuazonicacidandfreundsadjuvantinducedhistopathologicalandbiochemicalalterationsinthemousemodel