With the intensification of population aging, the topic of how to delay aging has garnered increasing attention in scientific circles. Chinese herbal medicine (CHM) boasts a long history of applications in delaying aging. Polysaccharides, a class of chemical substances with diverse biological activities derived from CHM, have recently attracted considerable interest for their potential anti-aging effects. While numerous studies have indicated that the anti-aging properties of polysaccharides from CHM are primarily attributed to their antioxidant activity, other mechanisms and effects remain to be systematically elucidated. This review aims to summarize the existing literature, providing a comprehensive overview that spans from the specific introduction of food and medicine homology (FMH) polysaccharides in CHM, to the analysis of the anti-aging mechanisms of polysaccharides derived from CHM, and further to the exploration of their activity in delaying aging and the underlying structure-activity relationships. It is elucidated that polysaccharides exhibit optimal anti-aging activity only within an appropriate molecular weight (Mw) range, and the anti-aging activities vary with different monosaccharide compositions and types of glycosidic bonds. Additionally, commonly utilized aging animal models in current research are also discussed. Overall, this review offers valuable insights into the anti-aging effects of polysaccharides from CHM and the corresponding regulatory mechanisms.

Hyperuricemia (HUA) has gradually become the fourth most prevalent chronic disease and the incidence rate is getting younger. In this study, Lophatherum gracile Brongn. with uric acid (UA)-lowering effects were screened from medicine food homology (MFH) plants by UA overproduction and excessive absorption cell models. Further, a murine model of potassium oxonate and yeast-induced HUA was used to evaluate the in vivo anti-high UA and nephroprotective effects of L. gracile, which significantly reduced serum UA and increased urine UA levels in HUA mice. L. gracile effectively inhibits the overproduction of UA by decreasing the activities of xanthine oxidase and adenosine deaminase (ADA), promoting excrement by regulating the mRNA expression of glucose transporter 9. Moreover, active components of L. gracile were analyzed by high-performance liquid chromatography-quadrupole time-of-flight mass spectrometry/mass spectrometry (HPLC-QTOF-MS/MS), network pharmacology was used to identify active ingredients further and validate targets. The results of network pharmacology showed that the components of the L. gracile acted on the targets xanthine dehydrogenase (XDH), adenosine deaminase (ADA), solute carrier family 2 member 9 (SLC2A9), and so on, which was consistent with the previous verification. The most likely active substances of L. gracile hydrojuglone glucoside. The effect of reducing UA is discovered for the first time in L. gracile. These findings suggested that L. gracile could be used as a potential confrontational strategy for the development of anti-HUA functional foods, providing the theoretical basis for the application of MFH plants and the development of related functional food products.

In the face of increasingly serious environmental pollution, the health of human lung tissues is also facing serious threats. Mogroside IIE (M2E) is the main metabolite of sweetening agents mogrosides from the anti-tussive Chinese herbal Siraitia grosvenori. The study elucidated the anti-inflammatory action and molecular mechanism of M2E against acute lung injury (ALI). A lipopolysaccharide (LPS)-induced ALI model was established in mice and MH-S cells were employed to explore the protective mechanism of M2E through the western blotting, co-immunoprecipitation, and quantitative real time-PCR analysis. The results indicated that M2E alleviated LPS-induced lung injury through restraining the activation of secreted phospholipase A2 type IIA (Pla2g2a)-epidermal growth factor receptor (EGFR). The interaction of Pla2g2a and EGFR was identified by co-immunoprecipitation. In addition, M2E protected ALI induced with LPS against inflammatory and damage which w ere significantly dependent upon the downregulation of AKT and mTOR via the inhibition of Pla2g2a-EGFR. Pla2g2a may represent a potential target for M2E in the improvement of LPS-induced lung injury, which may represent a promising strategy to treat ALI.