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Updated: May 11, 2026
Mouse Oocyte Microinjection, Maturation and Ploidy Assessment
Published on: July 23, 2011
Trimethylamine N-oxide Impairs Oocyte Maturation and Embryogenesis via NF-κB/NLRP3 Pathway Modulation
Fengping He1, Yongmei Zhang1, Yanle Guo2
1Institute of Reproductive Genetics, Dongguan Maternal and Child Health Hospital, No. 99, Zhenxing Road, Zhushan Community, Dongcheng District, Dongguan, Guangdong, 523002, China.
Background:
The role of Trimethylamine N-oxide (TMAO) in oocyte maturation and embryogenesis remains unclear, particularly its impact on ovarian granulosa cells (OGCs) and its underlying mechanisms.
Methods:
This study examined the effects of TMAO (100-400 μmol/L) on oocyte maturation, cumulus cell expansion, mitochondrial distribution, and embryonic development in vitro and in a BALB/c mouse model. The involvement of the NF-κB/NLRP3 signaling pathway in TMAO-induced ovarian dysfunction was assessed using Western blotting and gene expression analyses. The potential therapeutic effect of miRNA-146, an NF-κB inhibitor, was also explored.
Results:
Western blotting confirmed that TMAO activates the NF-κB signaling pathway and induces the synthesis of caspase 3 and NLRP3 complexes. However, pretreatment with miRNA-146, an NF-κB inhibitor, significantly reduced inflammation and inflammatory gene expression during TMAO therapy. Additionally, miRNA-146 pretreatment promoted oocyte maturation by suppressing NF-κB/NLRP3 activation, OGCs apoptotic inflammatory factor expression, and the gene expression of NF-κB, caspase 3, and NLRP3.
Conclusion:
Findings demonstrate that TMAO disrupts oocyte development through NF- κB/NLRP3 activation, contributing to ovarian dysfunction. Notably, targeting TMAO and its downstream signaling could serve as a novel therapeutic strategy for premature ovarian insufficiency (POI).
