Investigation of the effects of hesperidin administration on abamectin‐induced testicular toxicity in rats through oxidative stress, endoplasmic reticulum stress, inflammation, apoptosis, autophagy, and JAK2/STAT3 pathways

In this study, the potential effects of hesperidin (HES) on chronic toxicity caused by abamectin (ABM) in the testicular tissue were investigated through oxidative stress, inflammation, endoplasmic reticulum stress (ERS), apoptosis, and autophagy pathways. Male Sprague Dawley rats were used in the s...

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Bibliographic Details
Published inEnvironmental toxicology Vol. 37; no. 3; pp. 401 - 412
Main Authors Gur, Cihan, Kandemir, Ozge, Kandemir, Fatih Mehmet
Format Journal Article
LanguageEnglish
Published Hoboken, USA John Wiley & Sons, Inc 01.03.2022
Wiley Subscription Services, Inc
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Summary:In this study, the potential effects of hesperidin (HES) on chronic toxicity caused by abamectin (ABM) in the testicular tissue were investigated through oxidative stress, inflammation, endoplasmic reticulum stress (ERS), apoptosis, and autophagy pathways. Male Sprague Dawley rats were used in the study. Animals in the ABM group were orally administered 1 mg/kg ABM every other day for 28 days, while HES used against ABM was given at 100 or 200 mg/kg 30 min after ABM administration for 28 days. Markers of oxidative stress, inflammation, ERS, apoptosis, and autophagy in the testicular tissues removed after the animals are sacrificed were analyzed using biochemical, real‐time polymerase chain reaction (RT‐PCR), or western blot techniques. The results obtained showed that ABM caused oxidative stress, and triggered ERS, inflammation, apoptosis, and autophagy. On the other hand, HES showed antioxidant effect by increasing superoxide dismutase, catalase, glutathione peroxidase enzyme activities, and glutathione levels in testis tissue and attenuated lipid peroxidation. Accordingly, MAPK14 reduced the NF‐κB, IL‐1β, TNF‐α, and IL‐6 expression levels, presenting an anti‐inflammatory effect. In addition, Bax protected against apoptosis and autophagy by reducing the caspase‐3, beclin‐1, LC3A, and LC3B expressions, and increasing Bcl‐2 expression. It was observed that HES also interrupted the JAK2/STAT3 signaling pathway by suppressing IL‐6 expression. Taken into consideration together, HES provided significant protection against the destruction caused by ABM in testicular tissue with antioxidant, anti‐inflammatory, antiapoptotic, and anti‐autophagic effects. Thus, it was revealed that HES has the potential to serve as an alternative treatment option in ABM toxicity.
Bibliography:Funding information
Atatürk Üniversitesi, Grant/Award Number: TAB‐2021‐8926
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1520-4081
1522-7278
DOI:10.1002/tox.23406