The role of ginseng in aging: Insights into regulatory T cells activation and mitochondrial regulation

Abstract

A hallmark of aging is the progressive decline in resilience to stress and mitochondrial activity. As mitochondrial function decreases with aging, mitochondrial DNA (mtDNA) is shed under apoptotic stress, resulting in a persistent low-level of sterile inflammation (called inflammaging) that induces the aging program. In response to inflammaging, the body activates a compensatory anti-inflammatory response, including the activation of regulatory T (Treg) cells, to prevent excessive tissue damage. Recent studies have highlighted the dysfunction of Treg cells in elderly patients, suggesting that their critical role in the mitigation of aging. Additionally, mitochondrial electron transport chain (ETC) complexes, particularly complexes II and III, are essential for the function of Th1 and Treg cells, respectively. Since centenarians experience less inflammaging, this review aims to explore the anti-aging properties of ginseng. Research has shown that ginseng and its active compounds, ginsenosides, increase Treg cells population in aged mice and convert pro-inflammatory M1 macrophages into anti-inflammatory M2 macrophages. Furthermore, ginseng enhances antioxidant protein expression, decreases reactive oxygen species (ROS) production, restores mitochondrial ATP and membrane potential, and exerts anti-aging effects. Ginseng has been shown to extend lifespan, promote beneficial gut bacteria, and slow cognitive decline through its influence on immune cell circulation. Future research, including clinical trials, is needed to clarify the regulatory effects of ginseng on Treg cells, mitochondrial complexes, and their associated metabolites, as well as the interconnected mechanisms between them.