Deoxynivalenol triggers porcine intestinal tight junction disorder through hijacking SLC5A1 and PGC1α-mediated mitochondrial function

Xue, Dongfang; Yang, Ping; Yang, Yanyu; Wang, Yanan; Wu, Kuntan; Qi, Desheng; Wang, Shuai

doi:10.1016/j.fct.2022.112921

Cited by 24 publications

(10 citation statements)

References 48 publications

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“…Furthermore, abnormal mitochondrial energy metabolism may result in barrier damage. Reduced mitochondrial oxidative phosphorylation, adenosine triphosphate production, an abnormal glycolysis process, and lower cytochrome c levels were all linked to the breakdown of the cerebrovascular endothelial cell monolayer. , However, more research is needed to confirm whether NPs can induce barrier opening by influencing mitochondrial metabolism.…”

Section: Mechanisms Underlying Nanoparticle-induced Paracellular Rout...mentioning

confidence: 99%

How Nanoparticles Open the Paracellular Route of Biological Barriers: Mechanisms, Applications, and Prospects

Zhu

Liu

et al. 2022

ACS Nano

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Biological barriers are essential physiological protective systems and obstacles to drug delivery. Nanoparticles (NPs) can access the paracellular route of biological barriers, either causing adverse health impacts on humans or producing therapeutic opportunities. This Review introduces the structural and functional influences of NPs on the key components that govern the paracellular route, mainly tight junctions, adherens junctions, and cytoskeletons. Furthermore, we evaluate their interaction mechanisms and address the influencing factors that determine the ability of NPs to open the paracellular route, which provides a better knowledge of how NPs can open the paracellular route in a safer and more controllable way. Finally, we summarize limitations in the research models and methodologies of the existing research in the field and provide future research direction. This Review demonstrates the in-depth causes for the reversible opening or destruction of the integrity of barriers generated by NPs; more importantly, it contributes insights into the design of NP-based medications to boost paracellular drug delivery efficiency.

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Section: Mechanisms Underlying Nanoparticle-induced Paracellular Rout...mentioning

confidence: 99%

How Nanoparticles Open the Paracellular Route of Biological Barriers: Mechanisms, Applications, and Prospects

Zhu

Liu

et al. 2022

ACS Nano

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“…DON has attracted public attention due to its widespread pollution range and significant toxicological effects on humans and animals. Consumption of feed contaminated with DON causes intestinal damage of animals, possibly by inflammation, ROS accumulation, and oxidative stress . In this study, DON exposure to porcine intestinal epithelial cells IPI-2I induced an inflammatory response (TNF-α, ILs, and NLRP3 productions), oxidative stress (GPX4 and HO-1), and cell death.…”

Section: Discussionmentioning

confidence: 58%

“…Consumption of feed contaminated with DON causes intestinal damage of animals, possibly by inflammation, ROS accumulation, and oxidative stress. 39 In this study, DON exposure to porcine intestinal epithelial cells IPI-2I induced an inflammatory response (TNF-α, ILs, and NLRP3 productions), oxidative stress (GPX4 and HO-1), and cell death. It underscores the important role of LCA in protecting intestinal lesions and inflammation, as LCA intervention performed a drastic restoration in changes in cell number, inflammatory cytokines, the TNF-α/NF-κB pathway, p38/ERK-MAPK signals, and oxidative stress markers MDA and ROS in the DON-exposed IPI-2I cells.…”

Section: Discussionmentioning

confidence: 63%

Lithocholic Acid Alleviates Deoxynivalenol-Induced Inflammation and Oxidative Stress via PPARγ-Mediated Epigenetically Transcriptional Reprogramming in Porcine Intestinal Epithelial Cells

Li,

Zhu,

Yao

et al. 2024

J. Agric. Food Chem.

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Deoxynivalenol (DON) is a common mycotoxin that induces intestinal inflammation and oxidative damage in humans and animals. Given that lithocholic acid (LCA) has been suggested to inhibit intestinal inflammation, we aimed to investigate the protective effects of LCA on DON-exposed porcine intestinal epithelial IPI-2I cells and the underlying mechanisms. Indeed, LCA rescued DON-induced cell death in IPI-2I cells and reduced DON-stimulated inflammatory cytokine levels and oxidative stress. Importantly, the nuclear receptor PPARγ was identified as a key transcriptional factor involved in the DON-induced inflammation and oxidative stress processes in IPI-2I cells. The PPARγ function was found compromised, likely due to the hyperphosphorylation of the p38 and ERK signaling pathways. In contrast, the DON-induced inflammatory responses and oxidative stress were restrained by LCA via PPARγ-mediated reprogramming of the core inflammatory and antioxidant genes. Notably, the PPARγ-modulated transcriptional regulations could be attributed to the altered recruitments of coactivator SRC-1/3 and corepressor NCOR1/2, along with the modified histone marks H3K27ac and H3K18la. This study emphasizes the protective actions of LCA on DON-induced inflammatory damage and oxidative stress in intestinal epithelial cells via PPARγ-mediated epigenetically transcriptional reprogramming, including histone acetylation and lactylation.

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“…9 Considerable evidence suggests that DON exposure also induces ROS accumulation and reduces mitochondrial membrane potential (MMP; ΔΨ), impairing the mitochondrial structure, which corresponds to the dysfunction of TJs in the jejunum. 37,41 It has also been reported that AFB1 disrupts the integrity of the mitochondria (MMP and ROS), inducing mitochondrial dysfunction and impairing mitochondrial respiration in undifferentiated Caco-2 cells, an in vitro model of the human intestine. 42 In the present study, coexposure to ZEN, DON, and AFB1 caused mitochondrial damage, accompanied by the disruption of the mitochondrial morphological dynamics indicated by increase of mitochondrial fission and reduction of mitochondrial fusion.…”

Section: Papermentioning

confidence: 99%

Lycopene alleviates multiple-mycotoxin-induced toxicity by inhibiting mitochondrial damage and ferroptosis in the mouse jejunum

et al. 2022

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Deoxynivalenol triggers porcine intestinal tight junction disorder through hijacking SLC5A1 and PGC1α-mediated mitochondrial function

Cited by 24 publications

References 48 publications

How Nanoparticles Open the Paracellular Route of Biological Barriers: Mechanisms, Applications, and Prospects

How Nanoparticles Open the Paracellular Route of Biological Barriers: Mechanisms, Applications, and Prospects

Lithocholic Acid Alleviates Deoxynivalenol-Induced Inflammation and Oxidative Stress via PPARγ-Mediated Epigenetically Transcriptional Reprogramming in Porcine Intestinal Epithelial Cells

Lycopene alleviates multiple-mycotoxin-induced toxicity by inhibiting mitochondrial damage and ferroptosis in the mouse jejunum

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