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<p>High glucose (HG) conditions contribute to inflammation, oxidative stress, and DNA damage in monocytes, thereby promoting chronic disease progression. This study examines the protective effects of 6-gingerol, a major bioactive compound in ginger, against HG-induced cellular dysfunction in THP-1 monocytes. Treatment with 6-gingerol at concentrations of 30 and 60 µM significantly reduced the expression of inflammatory cytokines (IL-1β, TNF-α, and IL-6) at both the protein and mRNA levels, as demonstrated by Western blotting, qPCR, and ELISA. The compound also inhibited the activation of TLR2/4-mediated signaling pathways, including NF-κB, JAK/STAT3, and MAPK. Moreover, 6-gingerol mitigated HG-induced DNA damage by restoring phosphorylated levels of ATM, ATR, BRCA1, and p53 and normalized cell cycle regulation by modulating the expression of CDK4, Cyclin D1/E, and p21/p27. Cell viability assays (CCK-8, WST-1, and LDH) and FACS analyses (CFSE and Annexin V) confirmed no cytotoxic effects at 60 µM, suggesting that 6-gingerol offers protection without inducing cell death. A supplementary comparison with TLR4 inhibitors revealed a shared mechanism of action, further supporting the involvement of TLR4 in HG-induced pathogenesis. Collectively, these findings support 6-gingerol as a promising anti-inflammatory and cytoprotective agent under diabetic-like stress conditions.</p>

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6-Gingerol alleviates high glucose-induced inflammation and cytotoxicity in THP-1 cells by inhibiting TLR4 signaling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月7日

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  • Dong Young Kang,
  • Won-Jae Chi,
  • Jaehoon Cho,
  • Kyoung-Jin Jang

摘要

High glucose (HG) conditions contribute to inflammation, oxidative stress, and DNA damage in monocytes, thereby promoting chronic disease progression. This study examines the protective effects of 6-gingerol, a major bioactive compound in ginger, against HG-induced cellular dysfunction in THP-1 monocytes. Treatment with 6-gingerol at concentrations of 30 and 60 µM significantly reduced the expression of inflammatory cytokines (IL-1β, TNF-α, and IL-6) at both the protein and mRNA levels, as demonstrated by Western blotting, qPCR, and ELISA. The compound also inhibited the activation of TLR2/4-mediated signaling pathways, including NF-κB, JAK/STAT3, and MAPK. Moreover, 6-gingerol mitigated HG-induced DNA damage by restoring phosphorylated levels of ATM, ATR, BRCA1, and p53 and normalized cell cycle regulation by modulating the expression of CDK4, Cyclin D1/E, and p21/p27. Cell viability assays (CCK-8, WST-1, and LDH) and FACS analyses (CFSE and Annexin V) confirmed no cytotoxic effects at 60 µM, suggesting that 6-gingerol offers protection without inducing cell death. A supplementary comparison with TLR4 inhibitors revealed a shared mechanism of action, further supporting the involvement of TLR4 in HG-induced pathogenesis. Collectively, these findings support 6-gingerol as a promising anti-inflammatory and cytoprotective agent under diabetic-like stress conditions.