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Article 2023 · 16 atıf

Effects of chrysin in cadmium-induced testicular toxicity in the rat; role of multi-pathway regulation

Tuncer, Sibel Cigdem, Kucukler, Sefa, Gur, Cihan, Aygormez, Serpil, Kandemir, Fatih Mehmet

Özet

Background Cadmium (Cd) is a strong toxic agent and causes serious damage to testicular tissues. Chrysin (CHR) is a natural flavonoid with many effective properties, especially antioxidant, anti-inflammatory and anti-apoptotic properties. The current study describes new evidence for the ameliorative effects of CHR on oxidative stress, apoptosis, autophagy and inflammation pathways in Cd-induced testicular tissue toxicity. Methods Thirty-five male Wistar rats were divided into five groups, control, Cd, CHR, Cd + CHR25, and Cd + CHR50. Cd was administered alone at a dose of 25 mg/kg body weight or in combination with CHR 25 mg/kg and CHR 50 mg/kg for 7 days. Cd and CHR were administered orally. Biochemical, molecular, and histological methods were used to investigate inflammation, apoptosis, autophagy, and oxidant pathways in testicular tissue. Results Cd increased lipid peroxidation, JAK-2/STAT-3 levels, inflammation- related NF-kappa B, TNF-alpha, IL-1 beta, IL-6, COX-2, and iNOS levels, AKT-2, FOXO1, Bax, Apaf-1 and Caspase-3 levels, autophagic Beclin-1, LC3A and LC3B. The Cd also caused a decrease in the activities of antioxidant enzymes and GSH levels, antiapoptotic Bcl-2 levels. CHR, on the other hand, had the opposite effect of all these Cd-induced changes. Conclusions Overall, the data of this study indicate that testicular damage associated with Cd toxicity could be ameliorated by CHR administration.

Anahtar Kelimeler
Testicular toxicology Apoptosis Inflammation Cadmium Oxidative stress Chrysin OXIDATIVE STRESS HEPATOTOXICITY INFLAMMATION APOPTOSIS INJURY DAMAGE
WoS Kategorileri
Biochemistry & Molecular Biology
Sürdürülebilir Kalkınma Amaçları
Künye
Dergi
MOLECULAR BIOLOGY REPORTS
Yıl
2023
Cilt
50
Sayı
10
Sayfa
8305-8318
ISSN
0301-4851
eISSN
1573-4978
DOI
10.1007/s11033-023-08715-8
WoS UID
WOS:001051788000002
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