Abstract | OBJECTIVE: METHODS: HepG2 cells were induced by 50 mmol/L EtOH and 1 μg/mL LPS combined with YE intervention. The expression level of inflammatory cytokines was detected by ELISA. The expression level of TLR4 and the nuclear translocation of NF-κB were detected by immunofluorescence staining. The expression levels of TLR4, NF-κB, phospho-NF-κB-P65(P-NF-κB-p65), nucleus-phospho-NF-κB-p65(N-P-NF-κB-p65), tumor necrosis factor-α(TNF-α), interleukin-6(IL-6), and interleukin-1β(IL-1β) were detected by Western blot. RESULTS: Compared with the control group, the cells in EtOH+LPS group produced a large number of inflammatory factors and had a significant inflammatory response. YE intervention significantly alleviated EtOH+LPS induced hepatocyte inflammatory response. Further molecular mechanism studies showed that YE significantly reduced TLR4 expression level and inhibited NF-κB nuclear translocation in hepatocytes. CONCLUSION: YE can effectively inhibit the inflammatory response of HepG2 cells induced by EtOH and LPS, and its molecular mechanism may be related to the down-regulation of TLR4/NF-κB pathway.
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Authors | Lei Tian, Yan Zhang, Qian Cheng, Yanyang Han, Yajing Dong, Xiang Li, Hao Han |
Journal | Wei sheng yan jiu = Journal of hygiene research
(Wei Sheng Yan Jiu)
Vol. 53
Issue 1
Pg. 66-70
(Jan 2024)
ISSN: 1000-8020 [Print] China |
PMID | 38443174
(Publication Type: English Abstract, Journal Article)
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Chemical References |
- NF-kappa B
- Lipopolysaccharides
- Toll-Like Receptor 4
- Ethanol
- Interleukin-1beta
- Interleukin-6
- Tumor Necrosis Factor-alpha
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Topics |
- Humans
- Hep G2 Cells
- NF-kappa B
- Lipopolysaccharides
- Toll-Like Receptor 4
- Ethanol
(toxicity)
- Interleukin-1beta
- Interleukin-6
- Tumor Necrosis Factor-alpha
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