p38 mediates T-2 toxin-induced Leydig cell testosterone synthesis disorder

Yang, Xu; Song, Wenxi; Zhang, Kefei; Wang, Youshuang; Chen, Fengjuan; Chen, Yunhe; Huang, Tingyu; Jiang, Yibao; Wang, Xuebing; Zhang, Cong

doi:10.1016/j.ecoenv.2023.114695

Cited by 6 publications

(3 citation statements)

References 33 publications

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“…58 As an upstream molecule of NF-κB, JNK activates NF-κB to induce inflammation. 59 Therefore, we conclude that JNK activates NF-κB, which in turn causes IPEC-J2 cells to undergo an inflammatory response.…”

Section: The Mechanism Of T-2 Toxin Enterotoxicitymentioning

confidence: 74%

“…The results showed that addition of SP 600125 (a JNK inhibitor) significantly alleviated the functional impairment and inflammatory reaction induced by T-2 toxin, indicating that JNK activation mediated T-2 toxin-induced IPEC-J2 cell inflammation . As an upstream molecule of NF-κB, JNK activates NF-κB to induce inflammation . Therefore, we conclude that JNK activates NF-κB, which in turn causes IPEC-J2 cells to undergo an inflammatory response.…”

Section: Research Progress On the Enterotoxicity Of T-2 Toxinmentioning

confidence: 79%

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Overview of T-2 Toxin Enterotoxicity: From Toxic Mechanisms and Detoxification to Future Perspectives

Zhang,

Song,

Hua

et al. 2024

J. Agric. Food Chem.

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Fusarium species produce a secondary metabolite known as T-2 toxin, which is the primary and most harmful toxin found in type A trichothecenes. T-2 toxin is widely found in food and grain-based animal feed and endangers the health of both humans and animals. T-2 toxin exposure in humans and animals occurs primarily through food administration; therefore, the first organ that T-2 toxin targets is the gut. In this overview, the research progress, toxicity mechanism, and detoxification of the toxin T-2 were reviewed, and future research directions were proposed. T-2 toxin damages the intestinal mucosa and destroys intestinal structure and intestinal barrier function; furthermore, T-2 toxin disrupts the intestinal microbiota, causes intestinal flora disorders, affects normal intestinal metabolic function, and kills intestinal epidermal cells by inducing oxidative stress, inflammatory responses, and apoptosis. The primary harmful mechanism of T-2 toxin in the intestine is oxidative stress. Currently, selenium and plant extracts are mainly used to exert antioxidant effects to alleviate the enterotoxicity of T-2 toxin. In future studies, the use of genomic techniques to find upstream signaling molecules associated with T-2 enterotoxin toxicity will provide new ideas for the prevention of this toxicity. The purpose of this paper is to review the progress of research on the intestinal toxicity of T-2 toxin and propose new research directions for the prevention and treatment of T-2 toxin toxicity.

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Section: The Mechanism Of T-2 Toxin Enterotoxicitymentioning

confidence: 74%

Section: Research Progress On the Enterotoxicity Of T-2 Toxinmentioning

confidence: 79%

Overview of T-2 Toxin Enterotoxicity: From Toxic Mechanisms and Detoxification to Future Perspectives

Zhang,

Song,

Hua

et al. 2024

J. Agric. Food Chem.

Self Cite

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“…Multiple intracellular signaling pathways mediate the angiogenic response of endothelial cells, including vascular endothelial growth factor (VEGF)/VEGF receptor (VEGFR) signaling, TGF-β signaling and STAT signaling (4,6,7). In addition, all of the three major subfamilies of MAPK signaling, ERK, JNK and p38 MAPK, are involved in endothelial cell activation (8).…”

Section: Introductionmentioning

confidence: 99%

Complement factor H inhibits endothelial cell migration through suppression of STAT3 signaling

Jiang

Huang

et al. 2023

Exp Ther Med

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Complement factor H (CFH), a major soluble inhibitor of complement, is a plasma protein that directly interacts with the endothelium of blood vessels. Mutations in the CFH gene lead to diseases associated with excessive angiogenesis; however, the underlying mechanisms are unknown. The present study aimed to determine the effects of CFH on endothelial cells and to explore the underlying mechanisms. The adenoviral plasmid expressing CFH was transduced into HepG2 cells, and the culture medium supernatant was collected and co-cultured with human umbilical vein endothelial cells (HUVECs). Cell proliferation was measured by CCK8 and MTT assays, and cell migration was measured by wound healing and Transwell assays. Reverse transcription-quantitative PCR was performed to detect gene transcription. Western blotting was used to determine protein levels. The results revealed that CFH can inhibit migration, but not viability, of HUVECs. In addition, CFH did not significantly alter MAPK or TGF-β signaling, whereas it decreased STAT3 phosphorylation in HUVECs. Furthermore, CFH failed to reduce migration of HUVECs, with inhibition of STAT3 signaling by STATTIC or activation of STAT3 signaling by overexpression of STAT3 (Y705D) compromising CFH-inhibited HUVEC migration. CFH also decreased the expression levels of vascular endothelial growth factor receptor 2, a downstream effector of STAT3 mediating endothelial cell migration. In conclusion, the present study suggested that CFH may be a potential therapeutic target for angiogenesis-related diseases.

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Review of neurotoxicity of T-2 toxin

Wang,

Wang

et al. 2024

Mycotoxin Res

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p38 mediates T-2 toxin-induced Leydig cell testosterone synthesis disorder

Cited by 6 publications

References 33 publications

Overview of T-2 Toxin Enterotoxicity: From Toxic Mechanisms and Detoxification to Future Perspectives

Overview of T-2 Toxin Enterotoxicity: From Toxic Mechanisms and Detoxification to Future Perspectives

Complement factor H inhibits endothelial cell migration through suppression of STAT3 signaling

Review of neurotoxicity of T-2 toxin

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