RESUMEN
Dysregulation of lipid metabolism plays a key role in the onset and progression of CKD, and a thorough understanding of its regulatory mechanisms is essential for the development of effective treatments. In recent years, an increasing number of studies have focused on the pharmacological activities of natural products and their application in the treatment of chronic diseases. Natural products, including plant extracts and bioactive compounds, have been shown to exert anti-inflammatory, antioxidant, antifibrosis, and anti-apoptotic effects through various signaling pathways in the treatment of CKD. Many natural products have been shown to target dysregulated lipid metabolism through various signaling pathways. This review summarizes the key regulatory factors and signaling pathways involved in the dysregulation of lipid metabolism in chronic kidney disease (CKD), highlighting their importance as potential therapeutic targets. Recently published research on the potential therapeutic benefits of natural products for the treatment of CKD was described. These studies have revealed the multi-target role of natural products in the regulation of lipid metabolism. Natural products show great potential in targeting lipid metabolism-related pathways, offering a novel research direction for the treatment of CKD while providing a scientific basis and experimental support for the development of new treatment strategies.
RESUMEN
BACKGROUND AND AIM: Although the anti-cancer activity of isoalantolactone (IATL) has been extensively studied, the anti-melanoma effects of IATL are still unknown. Here, we have investigated the anti-melanoma effects and mechanism of action of IATL. MTT and crystal violet staining assays were performed to detect the inhibitory effect of IATL on melanoma cell viability. Apoptosis and cell cycle arrest induced by IATL were examined using flow cytometry. The molecular mechanism of IATL was explored by Western blotting, confocal microscope analysis, molecular docking, and cellular thermal shift assay (CETSA). A B16F10 allograft mouse model was constructed to determine the anti-melanoma effects of IATL in vivo. The results showed that IATL exerted anti-melanoma effects in vitro and in vivo. IATL induced cytoprotective autophagy in melanoma cells by inhibiting the PI3K/AKT/mTOR signaling. Moreover, IATL inhibited STAT3 activation both in melanoma cells and allograft tumors not only by binding to the SH2 domain of STAT3 but also by suppressing the activity of its upstream kinase Src. These findings demonstrate that IATL exerts anti-melanoma effects via inhibiting the STAT3 and PI3K/AKT/mTOR signaling pathways, and provides a pharmacological basis for developing IATL as a novel phytotherapeutic agent for treating melanoma clinically.