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Updated: Jul 19, 2025
An In Vivo Method to Study Mouse Blood-Testis Barrier Integrity
Published on: December 2, 2018
Deoxynivalenol Induces Blood-Testis Barrier Dysfunction through Disrupting p38 Signaling Pathway-Mediated Tight
Chenjiao Miao1, Zijia Wang1, Xin Wang1
1Heilongjiang Key Laboratory for Laboratory Animals and Comparative Medicine, College of Veterinary Medicine, Northeast Agricultural University, No. 600, Changjiang Road, Harbin 150030, China.
Abstract:
Deoxynivalenol (DON) is widely present in cereals and processed grains. It can disrupt the blood-testicular barrier (BTB), leading to sterility in males; however, the mechanism is unknown. In this study, 30 Kunming mice and TM4 cells were exposed to 0 or 4.8 mg/kg (28 d) and 0-2.4 μM (24 h) of DON, respectively. Histopathological findings showed that DON increased BTB permeability in mice, leading to tight junction (TJ) structural damage. Immunofluorescence results indicated that DON disrupted the localization of zonula occludens (ZO)-1. The results of protein and mRNA expression showed that the expression of ZO-1, occludin, and claudin-11 was reduced, and that the p38/GSK-3β/snail and p38/ATF-2/MLCK signaling pathways were activated in mouse testes and TM4 cells. Pretreatment with the p38 inhibitor SB203580 maintained TJ integrity in TM4 cells after exposure to DON. Thus, DON induced BTB dysfunction in mice by disrupting p38 pathway-mediated TJ expression and distribution.
