Lycopene alleviates zearalenone-induced oxidative stress, apoptosis, and NLRP3 inflammasome activation in mice kidneys.
Toxicon
; 249: 108078, 2024 Oct.
Article
de En
| MEDLINE
| ID: mdl-39181415
ABSTRACT
The aim of this study was to investigate the protective effects of lycopene on renal damage caused by zearalenone (ZEN). Male Kunming mice were treated daily for 4 weeks by intragastric administration with 40 mg/kg ZEN in the presence or absence of lycopene (2.5 or 5 mg/kg). The results showed that lycopene markedly alleviated the damage of renal structure and function in mice induced by ZEN, as indicated by the reduced degree of pathological damage and the decreased levels of urea nitrogen and creatinine. Meanwhile, results of dihydroethidine (DHE) staining and biochemical markers revealed that ZEN exposure notably increased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA), decreased the level of GSH, and reduced the activities of catalase (CAT) and superoxide dismutase (SOD). Administration of lycopene alleviated the increased oxidative stress induced by ZEN. Moreover, ZEN ingestion notably resulted in apoptosis, increased the protein levels of BCL2 associated X protein (Bax) and cleaved caspase-3, and decreased the protein levels of apoptosis regulator Bcl-2 (Bcl-2), which were reversed by lycopene intervention. Results of immunofluorescence demonstrated that lycopene reversed ZEN-induced the upregulation of NOD-like receptor pyrin domain-containing protein 3 (NLRP3), Caspase-1, and interleukin-1 beta (IL-1ß) in mice kidneys. Lycopene supplementation could alleviate ZEN-induced renal toxicity by inhibiting oxidative stress, apoptosis, and NLRP3 inflammasome activation.
Mots clés
Texte intégral:
1
Collection:
01-internacional
Base de données:
MEDLINE
Sujet principal:
Zéaralénone
/
Apoptose
/
Stress oxydatif
/
Inflammasomes
/
Protéine-3 de la famille des NLR contenant un domaine pyrine
/
Lycopène
/
Rein
Limites:
Animals
Langue:
En
Journal:
Toxicon
Année:
2024
Type de document:
Article
Pays d'affiliation:
Chine
Pays de publication:
Royaume-Uni