3-Hydro-2,2,5,6-tetramethylpyrazine: A novel inducer of zinc transporter-1 in HepG2 human hepatocellular carcinoma cells

Ishida, Tatsuro; Yamaguchi, Tadatoshi; Takechi, Seiji

doi:10.1016/j.abb.2015.07.002

Cited by 1 publication

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“…1) activates the nuclear factor erythroid 2-related factor 2-antioxidant (Nrf2-antioxidant) responsive element (ARE) pathway, and induces the mRNA and protein productions levels of heme oxygenase-1 (HO-1) and glutamate cysteine ligase catalytic subunit (Ishida et al, 2014). Moreover, DHP-3 also activates the metal-responsive transcription factor 1 pathway, and induces the mRNA and protein productions levels of zinc transporter-1 (Ishida et al, 2015). However, our current understanding is insufficient as to whether DHP-3 may also have an effect on other ROS-responsive signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

The effect of dihydropyrazines on lipopolysaccharide-stimulated human hepatoma HepG2 cells via regulating the TLR4-MyD88-mediated NF-κB signaling pathway

et al. 2020

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-Dihydropyrazines (DHPs), including 3-hydro-2,2,5,6-tetramethylpyrazine (DHP-3), are glycation products that are spontaneously generated in vivo and ingested via food. DHPs generate various radicals and reactive oxygen species (ROS), which can induce the expression of several antioxidant genes in HepG2 cells. However, detailed information on DHP-response pathways remains elusive. To address this issue, we investigated the effects of DHP-3 on the nuclear factor-κB (NF-κB) pathway, a ROS-sensitive signaling pathway. In lipopolysaccharide-stimulated (LPS-stimulated) HepG2 cells, DHP-3 decreased phosphorylation levels of inhibitor of NF-κB (IκB) and NF-κB p65, and nuclear translocation of NF-κB p65. In addition, DHP-3 reduced the expression of Toll-like receptor 4 (TLR4) and the adaptor protein myeloid differentiation primary response gene 88 (MyD88). Moreover, DHP-3 suppressed the mRNA expression of tumor necrosis factor-alpha (TNFα), and interleukin-1 beta (IL-1β). Taken together, these results suggest that DHP-3 acts as a negative regulator of the TLR4-MyD88-mediated NF-κB signaling pathway.

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Section: Introductionmentioning

confidence: 99%