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Ameliorative effect of curcumin loaded nanoliposomes: A Promising bioactive formulation, against the DBP-induced testicular damage.

作者信息

Bakeer Manal R, Rashad Maha M, Youssef Fady Sayed, Ahmed Omaima, Soliman Seham Samir, Ali Ghada E

机构信息

Physiology Department, Faculty of Veterinary Medicine, Cairo University, Giza 12211, Egypt.

Biochemistry and Molecular Biology Department, Faculty of Veterinary Medicine, Cairo University, Giza 12211, Egypt.

出版信息

Reprod Toxicol. 2025 Oct;137:109008. doi: 10.1016/j.reprotox.2025.109008. Epub 2025 Jul 22.

DOI:10.1016/j.reprotox.2025.109008
PMID:40706773
Abstract

Plasticizers are widely employed in various applications. Therefore, these products may have an impact on the biological systems of humans and other organisms. Thus, seeking a potent and eco-friendly protective agent becomes a great challenge. The current study investigated the underlying molecular mechanism associated with the protective effect of curcumin-loaded nanoliposomes (CUR nanoliposomes) against DBP-induced testicular damage. A total of twenty-four adult male rats were split up into four groups: the control group, the CUR nanoliposomes-treated group (100 mg/kg/day by oral gavage), the DBP-treated group (500 mg/kg/day by oral gavage), and the last group that received both treatments simultaneously for 60 days. The results showed that DBP exposure induced Leydig cell damage and testicular injury, represented by decreased serum sex hormone levels, downregulation of INSL3 gene expression, elevated testicular LDH, and aberrant sperm rate, as well as pathologically abnormal testicular anatomy. These testicular injuries are associated with redox state imbalance (elevated MDA, reduced CAT activity, and downregulation of Nrf2 and SOD gene expression), elevated apoptosis biomarkers (CASP3 and CASP9), and dysregulation of the PI3K/AKT/mTOR pathway. Co-administration of CUR nanoliposomes succeeded in reversing DBP-induced testicular damage. CUR nanoliposome-induced testicular protection could be attributed to the modulation of the PI3K/AKT/mTOR pathway.

摘要

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