Key Takeaways & Executive Findings
- •• TFL delays replicative and stress-induced cellular senescence and alleviates SASP. • TFL reduces bleomycin-induced DNA damage, pulmonary senescence, and fibrosis in mice. • Mechanistically, TFL suppresses p65 expression, inhibiting IL-1α/IL-1β and SASP. • TFL reverses bleomycin-induced gut microbiome alterations, suggesting a role in gut-lung axis.
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.
Idiopathic pulmonary fibrosis (IPF) is a relatively progressive interstitial lung disorder that leads to irreversible lung damage and ultimately death. Currently, there is no effective pharmacological treatment for IPF due to an incomplete understanding of the fundamental cellular and molecular mechanisms. IPF predominantly affects middle-aged and elderly populations and is correlated with increased mortality. Aging has been consistently identified as a significant risk determinant for IPF and is potentially linked to telomere shortening, mitochondrial dysfunction, and cellular senescence associated with the aging process. Studies have indicated a close connection between cellular senescence and the development of IPF and that elevated levels of IL-1α/IL-1β resulting from DNA damage or telomere dysfunction promote disease progression. In bleomycin-induced pulmonary fibrosis mouse models, IL-1α and IL-1β exert critical pro-inflammatory and pro-fibrotic effects by activating the NF-κB signaling pathway and stimulating myofibroblast differentiation, thereby driving the progression of fibrosis.
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LI Xiao-cui, WEI Yao, CHENG Qiu-cheng, XIAO Su-yu, YAO Si-si, YANG Dai-kang, WANG Ji-long, CHEN Li-ping, LI Qing, ZHAN Ting-zheng (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 are total flavonoids of litchi seed (TFL) and how do they affect aging?
TFL are natural compounds extracted from litchi seeds, rich in rutin and quercetin. This study shows that TFL delays cellular senescence by inhibiting the SASP through suppression of p65, thereby reducing inflammation and DNA damage.
How does TFL ameliorate pulmonary fibrosis?
TFL reduces bleomycin-induced pulmonary senescence and fibrosis by decreasing p21 protein levels and inhibiting the production of pro-inflammatory cytokines IL-1α and IL-1β via p65 suppression, thus alleviating fibrotic progression.
What is the molecular mechanism of TFL's anti-aging effect?
TFL suppresses the expression of p65, a key component of the NF-κB pathway, which in turn inhibits the secretion of SASP factors like IL-1α and IL-1β, thereby delaying cellular senescence.
Does TFL affect the gut microbiome?
Yes, bleomycin exposure alters the gut microbiome composition and function, and TFL treatment reverses these changes, suggesting a potential role in modulating the gut-lung axis.
What are the potential applications of TFL?
TFL shows promise as a natural anti-aging product and a therapeutic agent for age-related diseases such as idiopathic pulmonary fibrosis, though further clinical studies are needed.
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