Key Takeaways & Executive Findings
- •• TFL delays replicative and stress-induced cellular senescence and alleviates SASP. • TFL reduces DNA damage and counteracts bleomycin-induced pulmonary senescence and fibrosis. • Mechanistically, TFL suppresses p65 expression, inhibiting IL-1α/IL-1β and delaying senescence. • TFL reverses gut microbiome changes induced by bleomycin, suggesting a potential anti-aging therapeutic.
Abstract
Anti-aging foods not only benefit elderly individuals but also drive the development of safe and effective natural drugs. Here, we report that the addition of total flavonoids of litchi seed (TFL) delays replicative senescence and stress-induced senescence. TFL alleviates the senescence-associated secretory phenotype (SASP) and reduces the degree of DNA damage caused by bleomycin (BLM). TFL also counteracts stress-induced pulmonary senescence and fibrosis. TFL reduces the protein level of p21 in mouse lung and alleviates pulmonary fibrosis. Transcriptome profiling further reveals that TFL plays a key role in its anti-aging mechanism by inhibiting the SASP. Mechanistically, TFL suppresses p65 protein expression, thereby inhibiting IL-1α and IL-1β and delaying cellular senescence. Gut microbiome analysis reveals that the abundance and functions of the mouse gut microbiome change after BLM exposure and that TFL treatment reverses these changes. Overall, we provide a theoretical basis for the future application of TFL as a potential anti-aging product.
1. Introduction
Aging is a complex biological process involved in the development of various diseases, including cancer, cardiovascular diseases, Alzheimer’s disease, idiopathic pulmonary fibrosis, and type 2 diabetes. In modern society, with the increasing elderly population, the burden on healthcare systems and economic resources continues to grow. Therefore, preventing and managing age-related chronic diseases, as well as improving the health and quality of life of elderly individuals, holds significant social importance.
Research on aging can be traced back to cellular senescence mechanisms. Cellular senescence manifests as cell cycle arrest, increased activity of β-galactosidase, heightened DNA damage signals, and elevated p21 and p16 protein levels, along with an increase in the senescence-associated secretory phenotype (SASP). These changes are crucial cellular responses to various internal and external stressors, such as DNA damage, telomere shortening, and mitochondrial dysfunctions.
In 2025, Kroemer et al. identified fourteen key hallmarks of aging, including genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, extracellular matrix changes, altered intercellular communication, chronic inflammation, metabolic deregulation, and psychosocial isolation. Among these, the study of cellular senescence occupies a central position in understanding the mechanisms underlying aging. Cellular senescence promotes the secretion of SASP components, which release pro-inflammatory and pro-fibrotic factors that drive the initiation and progression of pulmonary fibrosis.
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Xiaocui Li, Yao Wei, Qiuchen Cheng, Suyu Xiao, Sisi Yao, Daikang Yang, Jilong Wang, Liping Chen, Qing Li, Tingzheng Zhan (2026). Total flavonoids of litchi seed attenuates cellular senescence by inhibiting the production of SASP through p65 suppression and ameliorates pulmonary fibrosis. Acta Biochimica et Biophysica Sinica. https://doi.org/10.3724/abbs.2025206
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Frequently Asked Questions
What is the main finding of this study?
The study demonstrates that total flavonoids of litchi seed (TFL) attenuate cellular senescence and pulmonary fibrosis by inhibiting SASP production through suppression of p65, thereby reducing IL-1α and IL-1β levels.
How does TFL affect cellular senescence?
TFL delays replicative and stress-induced senescence, alleviates SASP, reduces DNA damage, and counteracts bleomycin-induced pulmonary senescence and fibrosis.
What is the molecular mechanism of TFL action?
TFL suppresses p65 protein expression, which inhibits the production of IL-1α and IL-1β, key components of SASP, thereby delaying cellular senescence.
Does TFL influence the gut microbiome?
Yes, TFL treatment reverses changes in the abundance and functions of the mouse gut microbiome induced by bleomycin exposure, suggesting a potential role in gut health.
What are the potential clinical implications of this study?
The findings provide a theoretical basis for developing TFL as a natural anti-aging product and a potential therapeutic agent for idiopathic pulmonary fibrosis (IPF).
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