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Background <p>Sepsis-associated liver injury (SALI) is a risk factor for high mortality in patients with sepsis. However, the pathological mechanism and treatment strategies of SALI remain unclear. This study aims to explore the influence of lncRNA MIAT expression on SALI.</p> Results <p>The MIAT and TXNIP levels in the serum of SALI patients, RAW264.7 stimulated by LPS, and AML-12 co-cultured with RAW264.7 were increased, while miR-942-3p expression was decreased. The secretion level of inflammatory factors, the ROS positive rate, and the MDA content were increased, while the GSH levels and SOD enzymatic activity were reduced in LPS-stimulated RAW264.7. The activity of AML-12 was decreased, and the LDH level was increased. When the MIAT was inhibited, the above results showed opposite trends. MIAT was a molecular sponge for miR-942-5p and represses its activity. After inhibiting miR-942-5p, the inflammatory response and the oxidative stress level were enhanced in LPS-stimulated RAW264.7 and the damage of AML-12 was worsened.</p> Conclusions <p>The silence of MIAT alleviated the inflammatory response and oxidative stress in LPS-induced RAW264.7 and alleviated the damage of AML-12 cells by adsorbing miR-942-5p.</p>

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The LncRNA MIAT acts as a sponge for miR-942-5p to exacerbate the inflammation and oxidative stress in macrophages during sepsis-associated liver injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年5月30日

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  • Juanjuan Shi,
  • Zhiyuan Liu,
  • Juan Liu,
  • Enming Shi

摘要

Background

Sepsis-associated liver injury (SALI) is a risk factor for high mortality in patients with sepsis. However, the pathological mechanism and treatment strategies of SALI remain unclear. This study aims to explore the influence of lncRNA MIAT expression on SALI.

Results

The MIAT and TXNIP levels in the serum of SALI patients, RAW264.7 stimulated by LPS, and AML-12 co-cultured with RAW264.7 were increased, while miR-942-3p expression was decreased. The secretion level of inflammatory factors, the ROS positive rate, and the MDA content were increased, while the GSH levels and SOD enzymatic activity were reduced in LPS-stimulated RAW264.7. The activity of AML-12 was decreased, and the LDH level was increased. When the MIAT was inhibited, the above results showed opposite trends. MIAT was a molecular sponge for miR-942-5p and represses its activity. After inhibiting miR-942-5p, the inflammatory response and the oxidative stress level were enhanced in LPS-stimulated RAW264.7 and the damage of AML-12 was worsened.

Conclusions

The silence of MIAT alleviated the inflammatory response and oxidative stress in LPS-induced RAW264.7 and alleviated the damage of AML-12 cells by adsorbing miR-942-5p.