Succinate dehydrogenase inhibitor dimethyl malonate alleviates LPS/<scp>d</scp>-galactosamine-induced acute hepatic damage in mice

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  • Yongqiang Yang
    Department of Pathophysiology, Chongqing Medical University, PR China
  • Ruyue Shao
    Clinical Medical School, Chongqing Medical and Pharmaceutical College, PR China
  • Li Tang
    Department of Pathophysiology, Chongqing Medical University, PR China
  • Longjiang Li
    Department of Pathophysiology, Chongqing Medical University, PR China
  • Min Zhu
    Department of Pathology, Karamay Central Hospital, PR China
  • Jiayi Huang
    Department of Pathophysiology, Chongqing Medical University, PR China
  • Yi Shen
    Department of Pathophysiology, Chongqing Medical University, PR China
  • Li Zhang
    Department of Pathophysiology, Chongqing Medical University, PR China

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Description

<jats:p> In addition to its energy-supplying function, increasing evidence suggests that mitochondria also play crucial roles in the regulation of inflammation. Succinate dehydrogenase is also known as mitochondrial complex II, and inhibition of succinate dehydrogenase by dimethyl malonate has been reported to suppress the production of pro-inflammatory cytokines. In the present study, the potential anti-inflammatory benefits of dimethyl malonate were investigated in a mouse model with LPS/d-galactosamine-induced acute hepatic damage. Male BALB/c mice were injected i.p. with LPS and d-galactosamine to cause liver injury. The degree of liver injury, inflammatory response and oxidative stress and the survival of the experimental animals were determined. The results indicated dimethyl malonate decreased the level of aminotransferases in plasma, alleviated histological abnormalities in liver, inhibited the induction of TNF-α and IL-6 in plasma, suppressed hepatocyte apoptosis and improved the survival of LPS/d-galactosamine-exposed mice. Therefore, inhibition of succinate dehydrogenase by dimethyl malonate significantly alleviated LPS/d-galactosamine-induced hepatic damage, which suggests that succinate dehydrogenase might become a novel target for the intervention of inflammation-based hepatic disorders. </jats:p>

Journal

  • Innate Immunity

    Innate Immunity 25 (8), 522-529, 2019-08-31

    SAGE Publications

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