Baicalin attenuates hepatic injury in non-alcoholic steatohepatitis cell model by suppressing inflammasome-dependent GSDMD-mediated cell pyroptosis

Feb 7, 2020International immunopharmacology

Baicalin reduces liver cell damage in fatty liver disease by blocking inflammation-triggered cell death

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Abstract

Baicalin (BA) may improve hepatocyte health by reducing pyroptosis in a model of non-alcoholic steatohepatitis.

BA improves liver cell morphology and reduces cell death in a fatty acid-induced model of non-alcoholic steatohepatitis.
Treatment with BA leads to significant down-regulation of specific genes associated with inflammatory cell death, including NLRP3, GSDMD, and IL-1β.
BA decreases levels of proteins linked to inflammation and cell death, which may reduce pyroptosis.
The protective effects of BA are diminished when GSDMD is knocked down, suggesting its role in mediating BA's effects.

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Baicalin (BA), a flavone glycoside, is the constituent of Scutellaria baicalensis, a Chinese herbal medicine used to treat non-alcoholic steatohepatitis (NASH). However, the mechanism of BA on NASH is still not clear. Here, the improving effect of BA on hepatocyte through inhibition of pyroprosis was investigated in vitro. With a cell model of NASH exposing HepG2 cells in free fatty acids (FFA), we revealed that BA could improve hepatocyte from FFA-induced morphological damage and death. And then through transcriptomes screening, a significant down-regulation of NLR pyrin domain containing 3 (Nlrp3), gasdermin D (Gsdmd), andinterleukin-1 beta (IL-1β) expression were found after BA treatment. Further analysis confirmed that BA could decrease the levels of NLRP3 and GSDMD, as well as the release of IL-1β and IL-18, resulting in the reduction of pyroptosis. Moreover, the improving effect of BA could be attenuated by Gsdmd knockdown. In conclusion, BA can reduce pyroptosis of hepatocyte by blocking NLRP3-GSDMD signaling in vitro.

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Baicalin attenuates hepatic injury in non-alcoholic steatohepatitis cell model by suppressing inflammasome-dependent GSDMD-mediated cell pyroptosis

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