20(S)-Ginsenoside-Rg3

The risk of exposure to particulate matter (PM) has been consistently highlighted globally owing to its detrimental effects on the respiratory and cardiovascular systems and in the development of lung cancer. Additionally, PM promotes cancer cell metastasis; however, research elucidating the precise mechanisms underlying this phenomenon and the strategies to inhibit it remains limited. The aim of this study was to elucidate the mechanism underlying PM-induced cancer metastasis and investigate the preventive role of ginsenoside Rg3. We treated macrophages with PM and confirmed an increase in the expression and secretion of chemokines, such as CCL3, CCL4, and CCL5. This effect was mediated by the MAPK and NF-kB pathways, and Rg3 inhibited this process by suppressing chemokine expression. These chemokines regulate the expression of epithelial-mesenchymal transition (EMT) markers in cancer cells, including Snail, Slug, ZEB1, and E-cadherin. The regulated EMT markers increased the motility of cancer cells in vitro. Furthermore, an increase in CCL3, CCL4, and CCL5 in the bronchoalveolar lavage fluid (BALF) was confirmed in a PM inhalation mouse model, and Rg3 reduced PM-induced cancer metastasis. The study findings suggest the potential use of Rg3 as a therapeutic agent to prevent PM-induced cancer metastasis.

This study aimed to investigate the protective mechanism of Ginsenoside Rg3 (Rg3) against Di-n-butyl phthalate (DBP) induced spermatogenic damage, focusing on the Src/PI3K/Akt pathway. In vivo experiments demonstrated that Rg3 restored DBP-induced dysregulation of gap junction (GJ) protein connexin 43 (Cx43), improved testicular structure, enhanced sperm parameters (count and motility), and upregulated phosphorylation of Src, PI3K, and Akt (p-Src, p-PI3K, p-Akt) in mice. In vitro studies, using the metabolite of DBP, monobutyl phthalate (MBP), and pathway inhibitors (PP2 for Src and LY294002 for PI3K), further confirmed these effects. Rg3 increased antioxidant enzyme activity, reduced oxidative stress marker MDA, and enhanced the expression of p-Src, p-PI3K, p-Akt, and Cx43 in MBP-treated TM4 Sertoli cells. Inhibitor experiments confirmed that the Src/PI3K pathway mediates Rg3's protective action. These findings suggest that Rg3 alleviates DBP/MBP-induced male reproductive dysfunction by enhancing antioxidant capacity and reactivating the Src/PI3K/Akt signaling pathway, which helps restore blood-testis barrier (BTB) integrity through Cx43 stabilization. Thus, Rg3 may serve as a potential therapeutic agent for environmental toxicant-related male infertility.