Eleutheroside E

Wu‐Teng Decoction (WTD) is a significant in‐hospital preparation widely used in clinical practice to treat rheumatoid arthritis (RA) in China, however, its active substances and underlying mechanisms remain unclear. In this study, the chemical constituents of WTD were analyzed using ultra‐high‐performance liquid chromatography‐tandem mass spectrometry, identifying a total of 120 compounds, including flavonoids, phenylpropanoids, phenolic acids, alkaloids, etc. Subsequently, network pharmacology analyses revealed that 29 compounds were potential active compounds in WTD for the treatment of RA, as well as 48 core anti‐RA targets, including tumor necrosis factor‐α, V‐Akt murine thymoma viral oncogene homolog 1, and albumin. Further analysis suggested that WTD treats RA via the phosphoinositide 3‐kinase‐Akt, mitogen‐activated protein kinase, and Ras signaling pathways. Molecular docking analysis of the top five pivotal targets with the core active ingredients demonstrated suitable binding interactions at the active site of target proteins. The significant reduction of nitric oxide levels in lipopolysaccharides‐induced RAW264.7 cells validated the anti‐inflammation activity of WTD.

Alzheimer's disease (AD) is a common neurodegenerative disorder, and oxidative stress plays a significant role in its progression. Owing to its nourishing effects, Eleutherococcus senticosus (Rupr. & maxim.) maxim. (ES) has gained widespread popularity globally as a functional food and long-term consumption has been shown to enhance memory. The phenylpropanoid components extracted from Eleutherococcus senticosus (Rupr. & maxim.) maxim. (ESP) exhibit a diverse array of bioactivities and are commonly employed in the treatment of central nervous system (CNS) disorders. Nonetheless, the exact mechanisms by which ESP alleviates oxidative stress in AD models require further investigation. Therefore, this study utilized SAMP8 mice as models for AD and employed L-glutamate (L-Glu)-induced HT22 cells to establish an in vitro AD model. The effects of ESP on cognitive function were evaluated using the Morris water maze (MWM) test. Additionally, various techniques such as pathology, immunofluorescence staining (IF), ROS staining, cellular thermal shift assay (CETSA), Mst1 inhibitor analysis, and western blotting (WB) were conducted to further investigate the pharmacological efficacy and potential molecular mechanisms of ESP. In vivo, ESP was found to improve cognitive function in SAMP8 mice and alleviate AD-like pathological features. In vitro, ESP reduced intracellular ROS levels. Mechanistically, CETSA analysis confirmed the binding affinity between ESP and Mst1, demonstrated that ESP modulated the Mst1 signaling pathway to mitigate oxidative stress and decrease ROS levels. These findings suggested that ESP holded significant potential for developing therapeutic strategies for AD.