Targeting MLKL ameliorates T-2 toxin-induced cartilage damage by inhibiting chondrocyte death and matrix degradation in mice.

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Tác giả: Jinghong Chen, Yinan Liu, Yue Liu, Yawen Shi, Meng Zhang, Ying Zhang, Xiaoru Zhao

Ngôn ngữ: eng

Ký hiệu phân loại: 305.568 +Alienated and excluded classes

Thông tin xuất bản: Germany : Archives of toxicology , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 201326

T-2 toxin is the most toxic mycotoxin found in contaminated food and animal feed that threatens health. Exposure to T-2 toxin causes cartilage damage and leads to joint disorders, but the mechanisms underlying T-2 toxin-induced cartilage damage remain unclear. The results showed that T-2 toxin-induced chondrocyte death in articular cartilage from rats fed T-2 toxin (200 ng/g b.w./day) caused a significant increase in phosphorylated receptor-interacting protein 3 (p-RIPK3) and phosphorylated mixed lineage kinase-like protein (p-MLKL). In vitro studies showed that T-2 toxin (48 ng/mL) reduced the viability of C-28/I2 chondrocytes, increased cell apoptosis, and significantly upregulated the expression of p-MLKL. The results suggest that chondrocyte necroptosis is involved in T-2 toxin-induced cartilage damage. Furthermore, necrostatin-1 (Nec-1), a necroptosis inhibitor, significantly attenuated T-2 toxin-induced cell death and the increase of p-MLKL. Further studies showed that mlkl
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