The role of JAK2/STAT3 pathway in non-cytotoxic concentrations of DON-induced aggravation of inflammatory response in IL-10 deficient RAW264.7 cells

Zeng, Junya; Lin, Ziman; Tang, Jiangyu; Chen, Xingxiang; Huang, Kehe; Gan, Fang

doi:10.1016/j.fct.2024.114557

Cited by 2 publications

(1 citation statement)

References 41 publications

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“…Therefore, DON contamination is a major issue for food and feed safety globally . DON poses a serious threat to animal and human health due to its multiple harmful effects, including liver damage, immune system damage, reproductive toxicity, and more. ,, Therefore, the European Commission had set the maximum level of DON in processed cereals and infant meals at 1250 and 200 μg/kg, respectively . To investigate the effects of low-dose DON exposure on organisms, 200 μg/kg DON was selected for this study.…”

Section: Discussionmentioning

confidence: 99%

Hesperidin Alleviates Hepatic Injury Caused by Deoxynivalenol Exposure through Activation of mTOR and AKT/GSK3β/TFEB Pathways

Wang,

Chen,

Jiang

et al. 2024

J. Agric. Food Chem.

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Section: Discussionmentioning

confidence: 99%

Hesperidin Alleviates Hepatic Injury Caused by Deoxynivalenol Exposure through Activation of mTOR and AKT/GSK3β/TFEB Pathways

Wang,

Chen,

Jiang

et al. 2024

J. Agric. Food Chem.

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HMGB1/TREM1 crosstalk between heat-injured hepatocytes and macrophages promotes HCC progression after RFA

Xiong,

Li,

Hong

et al. 2024

J Cancer Res Clin Oncol

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Purpose Tumor recurrence after radiofrequency ablation (RFA) affects the survival rate of patients and limits its clinical application. Tumor recurrence around the ablation area may be related to the thermal injury of hepatocytes (HCs) around the tumor, but the specific mechanism is still unclear. Methods A liver cancer thermal injury mouse model was established via RFA in the C57BL/6 mice. Primary HCs and Kupffer cells (KCs) were isolated and cultured to assess their sensitivity to thermal injury via the MTT assay. Flow cytometry was used to assess macrophage polarization. Furthermore, Western blotting and co-immunoprecipitation (co-IP) were utilized to evaluate the protein expression of intracellular signaling pathway. Finally, Transwell and wound healing assays was conducted to evaluate the invasion potential of liver cancer cells. Results Our findings revealed that RFA-induced liver thermal injury promoted the upregulation and secretion of HMGB1 in HCs. HMGB1 had a protective effect on HCs thermal injury, potentially mediated through autophagy regulation. Heat-injured HCs release HMGB1, which activates the TREM1/JAK2/STAT3 signaling pathway in KCs, thus fostering an immunosuppressive tumor microenvironment (TME). Moreover, HMGB1 secretion by heat-injured HCs exacerbates the migration and invasion of HCC cells by influencing macrophage polarization. Conclusion RFA-induced thermal injury triggers HMGB1 release from HCs, driving macrophage M2 polarization and increasing the invasion ability of liver cancer cells. These findings reveal a potential therapeutic target for combating liver cancer recurrence following thermal ablation.

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The role of JAK2/STAT3 pathway in non-cytotoxic concentrations of DON-induced aggravation of inflammatory response in IL-10 deficient RAW264.7 cells

Cited by 2 publications

References 41 publications

Hesperidin Alleviates Hepatic Injury Caused by Deoxynivalenol Exposure through Activation of mTOR and AKT/GSK3β/TFEB Pathways

Hesperidin Alleviates Hepatic Injury Caused by Deoxynivalenol Exposure through Activation of mTOR and AKT/GSK3β/TFEB Pathways

HMGB1/TREM1 crosstalk between heat-injured hepatocytes and macrophages promotes HCC progression after RFA

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