Published online Nov 7, 2020. doi: 10.3748/wjg.v26.i41.6346
Peer-review started: May 19, 2020
First decision: July 29, 2020
Revised: July 30, 2020
Accepted: August 29, 2020
Article in press: August 29, 2020
Published online: November 7, 2020
Chronic liver injury (CLI) is the beginning of many serious liver diseases. If not timely managed CLI can seriously threaten human health. It has been reported that pyroptosis occurs in CLI. However, there is no drug that reduces CLI by regulating pyroptosis.
To explore the therapeutic effect and mechanism of dihydromyricetin (DHM) on CLI from a new perspective of the pathogenesis of CLI-pyroptosis.
We mainly focused on the regulatory effect of DHM on pyroptosis in CLI. The effect of DHM on pyroptosis was evaluated at the following three levels: Morphology, protein and mRNA. The related mechanism of DHM treatment for CLI was also studied.
A CLI mouse model was established by subcutaneous injection of carbon tetrachloride (CCl4) into the back. After establishment of the model, the therapeutic effect of DHM on CLI was estimated by serological detection, HE staining and ORO staining. Western blotting, immunohistochemistry and qRT-PCR were used to detect the changes in pyroptosis-related molecules.
DHM improved liver damage caused by CCl4, reduced steatosis in hepatocytes, and inhibited the pyroptosis signal.
DHM can improve CCl4-induced CLI and regulate the pyroptosis pathway in hepatocytes. DHM may be a potential therapeutic drug for CLI.
As a newly discovered programmed cell death, pyroptosis provides a new direction for the study of the pathogenesis of CLI. DHM affects the mechanism of action by regulating pyroptosis to alleviate CLI. This could be a major breakthrough in the development of drugs for CLI.