TAGRA 2025

Exosomes released from cancer cells are nano-vesicles that play a critical role in reshaping the tumor microenvironment and disrupting the functions of distant cellular targets. Through their cargo—oncogenic miRNAs, pro-inflammatory proteins, tumor-specific metabolites, and DNA/RNA fragments—they alter intercellular communication pathologically. Exosome-mediated damage compromises both central nervous system barrier integrity and neuronal function, thereby providing an indirect yet significant contribution to cancer progression. Current therapeutic approaches remain insufficient in reducing this toxicity and inflammation. In recent years, studies on Panax ginseng have revealed notable effects, particularly in suppressing oxidative stress and apoptosis. Moreover, ginseng has been shown to attenuate responses to pro-inflammatory mediators such as IL-6 and TNF-α induced by exosomes, and to exert anti-inflammatory activity by reducing intracellular NF-κB activation. More realistic evaluation of exosome-mediated toxicity and treatment effects is achievable through co-culture models that physiologically reflect neuron–endothelial interactions. A co-culture model was established using HUVEC and SH-SY5Y cells. Following incubation, cancer-derived exosomes obtained from the T98G cell line (40 ng/mL) were applied to the co-culture system to induce exosome-mediated toxicity. Ginseng was then administered as a therapeutic agent at doses of 200 ng/mL and 400 ng/mL. At the end of the treatment period, cellular viability (MTT assay) and oxidative stress markers (TAC and TOS) were evaluated. Treatment with 400 ng/mL ginseng reduced oxidative stress and inflammation compared with the exosome control group and increased cell viability by approximately 30%. Our study shows that ginseng may serve as a therapeutic agent capable of counteracting the harmful effects of cancer-derived exosomes on neuronal and endothelial cells. This highlights its potential in mitigating exosome-mediated toxicity within the context of neuro-oncological damage.