NINGBO INNO PHARMCHEM CO.,LTD. is proud to highlight the extensive research into Dihydromyricetin (DHM), also known as Ampelopsin. This natural flavanonol, primarily sourced from Vine Tea (Ampelopsis grossedentata), is garnering significant attention for its profound effects on liver health. As scientific investigations continue, the intricate mechanisms by which DHM ameliorates liver fibrosis and protects liver cells are becoming clearer.

One of the primary ways DHM supports liver health is through its ability to induce autophagy in hepatic stellate cells (HSCs). Liver fibrosis, a complex process characterized by the excessive deposition of extracellular matrix, is a major contributor to liver diseases. HSCs play a pivotal role in this process. Research indicates that DHM treatment effectively inhibits the activation of these stellate cells by promoting autophagy, a cellular 'clean-up' mechanism. Studies have shown that DHM administration leads to an increase in key autophagy-related markers, suggesting that this process is integral to its antifibrotic effects. By initiating autophagic flux, DHM helps in the inactivation of HSCs, thereby slowing down or reversing fibrotic progression.

Beyond its direct impact on HSCs, DHM also demonstrates a remarkable ability to modulate the immune microenvironment within the liver. Specifically, it enhances the activity of hepatic natural killer (NK) cells. NK cells are crucial components of the immune system that can target and eliminate damaged or abnormal cells. In the context of liver fibrosis, activated NK cells can release cytokines, such as interferon-gamma (IFN-γ), which are known to have antifibrotic properties. Scientific findings reveal that DHM administration increases the frequency and activation of hepatic NK cells, and importantly, boosts their production of IFN-γ. This enhanced NK cell-mediated killing of activated HSCs further contributes to the protective effects of DHM against liver fibrosis.

The intricate signaling pathways involved in DHM's action are also being elucidated. Research points to the aryl hydrocarbon receptor (AhR) as a key player, which, in conjunction with NF-κB and STAT3 signaling pathways, regulates IFN-γ production in NK cells. DHM appears to activate the AhR, which in turn influences these downstream pathways, ultimately leading to increased IFN-γ secretion. This multi-faceted approach—combining direct inactivation of fibrotic cells through autophagy and indirect immune support via NK cell activation—underscores the comprehensive benefits of DHM for liver health. Understanding these mechanisms allows for more targeted applications of dihydromyricetin for liver fibrosis prevention and treatment.

For those seeking natural solutions to support liver function and combat the effects of liver fibrosis, dihydromyricetin stands out as a promising compound with a strong scientific backing. Its capacity to promote autophagy and enhance immune responses makes it a valuable ingredient in health supplements designed for liver care.