Aging involves not only oxidative damage, inflammation, mitochondrial dysfunction, and DNA damage, but also the accumulation of senescent “zombie cells” that can release harmful inflammatory signals. A 2026 study published in Nature Communications found that the natural flavonoid dihydromyricetin (DHM) targets PRDX2, helping reduce DNA damage and the senescence-associated secretory phenotype (SASP). Cellular and animal studies also showed potential effects on different types of senescent cells. While these findings remain limited to preclinical research, they highlight a promising new research direction for dihydromyricetin and vine tea polyphenols in cellular senescence intervention.
Why do humans age? It seems like a question everyone knows the answer to, yet it remains a question that science has never been able to fully explain.
We know that as we grow older, oxidative damage gradually accumulates in the body, inflammatory activity may change, mitochondrial function progressively declines, and DNA damage becomes increasingly difficult to repair. Behind these changes, however, another distinctive form of “aging” is quietly taking place. Some cells do not die, but gradually lose their ability to function normally. They stop dividing without being promptly cleared by the body. Even more importantly, these cells continuously release inflammatory signals and other factors that can affect surrounding cells and tissues. Scientists have vividly described them as “zombie cells,” or senescent cells.
This raises an increasingly important question: If we could actively remove or modulate these senescent cells, could we potentially intervene in the aging process from another perspective? In 2026, researchers turned their attention to a natural flavonoid from traditional vine tea—dihydromyricetin.
Food Ingredient: Ampelopsis grossedentata Leaf Polyphenols
In 2026, the National Health Commission of China issued an announcement regarding 16 “Three New Foods,” including peony seed oil and other substances. Among them, Ampelopsis grossedentata leaf polyphenols were officially approved as a new food ingredient.
It is worth noting that during the application process, this ingredient was previously referred to as “vine tea polyphenols” and was later renamed “Ampelopsis grossedentata leaf polyphenols.”
According to official information, the ingredient is produced using the leaves of Ampelopsis grossedentata, a plant belonging to the genus Ampelopsis in the grape family. The manufacturing process involves ethanol extraction, decolorization, concentration, filtration, drying, and other procedures. Its major components include dihydromyricetin and other polyphenolic compounds, with a total polyphenol content of no less than 85%.
Among these polyphenols, dihydromyricetin (DHM) is particularly noteworthy. It is a representative flavonoid compound found in the leaves of Ampelopsis grossedentata and has long been one of the major active compounds receiving attention in vine tea research.
Research: Dihydromyricetin and Senescent Cells
In the past, research on dihydromyricetin mainly focused on areas such as antioxidant activity, anti-inflammatory effects, and glucose and lipid metabolism. However, a new study in 2026 marked an interesting shift in the research landscape.
The study was published in the international journal Nature Communications under the title The natural flavonoid dihydromyricetin targets senescent cells via PRDX2 and alleviates age-related diseases. The research was led by a Chinese scientific team. Researchers from the School of Medicine at Shanghai Jiao Tong University were primarily involved in studies of cellular senescence, molecular mechanisms, and animal experiments. The Shanghai Institute of Nutrition and Health, Chinese Academy of Sciences, has long conducted research related to nutrition, aging, and disease. James L. Kirkland and his team from Cedars-Sinai Medical Center in the United States have also conducted extensive research on senescent cells, aging interventions, and age-related diseases.
Rather than focusing on “antioxidant activity” in the traditional sense, the study investigated a question that has received increasing attention in the field of aging biology in recent years: Can senescent cells become a target for interventions against aging and age-related diseases?
Nature
1) Screening 50 Natural Molecules
Aging may involve much more than the continuous accumulation of oxidative damage. A population of functionally abnormal senescent cells can also gradually accumulate in the body. This raises another question: Can natural compounds directly intervene in these cells?
The research team did not simply assume that dihydromyricetin was the answer. Instead, they began with a screening process involving natural compounds.
They used a candidate library containing 50 natural medicinal agents (NMA), most of which were derived from plants. The researchers then established an in vitro cellular senescence screening system and individually exposed senescent cells to these 50 natural medicinal agents. The compounds were evaluated from two perspectives: first, whether they could alter the secretory phenotype of senescent cells, known as the senescence-associated secretory phenotype (SASP); and second, whether they could selectively kill senescent cells.
The screening results showed that some compounds could significantly suppress SASP, including dihydromyricetin.
Further concentration-dependent experiments found that higher concentrations of dihydromyricetin produced cytotoxic effects on both normal and senescent cells. At lower effective concentrations, however, dihydromyricetin significantly reduced SASP while preserving characteristic features of cellular senescence, including cell-cycle arrest.
In other words, rather than simply causing senescent cells to resume proliferation, dihydromyricetin appeared to alter the “senescent state” of these cells and reduce their potentially harmful effects on surrounding tissues.
This type of activity is generally described in aging research as senomorphic activity, referring to the modulation of the senescent phenotype.
Based on these findings, the researchers initially identified dihydromyricetin as a promising candidate for further investigation as a senomorphic compound.
2) Dihydromyricetin and the PRDX2 Protein
After confirming that dihydromyricetin was effective, a more critical question emerged: Which protein inside the cell does it directly act on?
To answer this question, the research team used a proteomic approach. They exposed dihydromyricetin to a large number of different human proteins to determine which proteins it could interact with.
After two rounds of screening and cross-validation, the number of candidate proteins was progressively narrowed down. Ultimately, the researchers focused on a protein called PRDX2 (peroxiredoxin 2).
PRDX2 is a protein involved in maintaining cellular redox balance. Previous research has primarily focused on its role in helping cells respond to oxidative stress. In this study, however, researchers identified another phenomenon: binding with dihydromyricetin could affect the cellular localization of PRDX2.
Specifically, PRDX2 does not normally tend to accumulate extensively in the cell nucleus, whereas dihydromyricetin could promote its movement into the nucleus.
The cell nucleus contains DNA, and senescent cells face a particularly important problem: DNA damage continues to accumulate without being adequately repaired.
The researchers further found that after dihydromyricetin promoted the movement of PRDX2 into the nucleus, PRDX2 could help cells process this DNA damage. As signals associated with DNA damage decreased, the release of SASP from senescent cells also declined.
A complete causal pathway gradually emerged:
Dihydromyricetin binds to PRDX2 → promotes the movement of PRDX2 into the cell nucleus → helps the cell process DNA damage → ultimately reduces the harmful signals released by senescent cells.
To further demonstrate that PRDX2 was indeed a key component of this mechanism, the researchers reduced PRDX2 levels in the cells. The results showed that when PRDX2 was reduced, the effects of dihydromyricetin were also significantly weakened. This provided further support for the important role of PRDX2 in the process.
3) Animal and Cellular Experiments
The researchers further found that dihydromyricetin may produce different effects on different types of senescent cells.
In fibroblasts, it primarily appeared to improve the abnormal state of senescent cells and reduce the inflammatory signals they released.
In senescent microglia, however, differences in PRDX2 levels and cellular states meant that dihydromyricetin could instead further affect mitochondrial function and promote the death of these senescent cells.
In other words, dihydromyricetin may have an interesting dual effect: for some senescent cells, it may help “quiet them down,” while for other senescent cells, it may potentially help eliminate them.
Finally, the research team moved beyond cellular experiments to animal models.
In prematurely aging mice, dihydromyricetin improved certain age-related changes. In an Alzheimer’s disease mouse model, it also reduced some senescent microglia and improved certain disease-related manifestations.
Of course, these findings are currently based primarily on cellular and animal experiments and cannot be directly equated with anti-aging effects in humans.
Nevertheless, from the perspective of food ingredient research, the findings open an interesting new direction for vine tea polyphenols and dihydromyricetin—moving beyond traditional antioxidant research toward the emerging field of cellular senescence intervention.
References
Qixia Xu, Gaoxiang Li, Hongwei Zhang, et al. The natural flavonoid dihydromyricetin targets senescent cells via PRDX2 and alleviates age-related diseases. Nature Communications. 2026;17:3936.