The potential therapeutic role of ginsenosides on fibrosis-associated diseases: A review on molecular mechanisms and call for further research

Fibrosis is often defined as a dysregulated reparative process of direct replacement of dead or damaged cells with connective tissue, resulting in progressive architectural remodeling in nearly all tissues and organs. Consequently, the burden of fibrosis is significant, with relatively high morbidity and mortality. Ginseng (Panax ginseng C. A. Meyer), owing to its medicinal properties, has been utilized in Chinese patent medicines as a principal component to attenuate fibrotic diseases. As the major bioactive compounds of ginseng, ginsenosides have gained much interest. In the recent five years, significant pharmaceutical potential of ginsenosides has been extensively studied in a variety of organ fibrosis diseases such as liver fibrosis, myocardial fibrosis, renal fibrosis and pulmonary fibrosis. Ginsenosides have been elucidated to exhibit potential effects on inflammatory response resulting from parenchymal cell damage, activation of myofibroblasts to produce ECM and apoptosis or inactivation of myofibroblasts. Correspondingly, potential downstream targets or pathways of these pathological processes have also been identified to be affected by ginsenosides. This review provides an overview of effective treatments of ginsenosides on various tissue fibrosis and their possible anti-fibrotic mechanisms, further proffering a reference of developing new candidate drugs for the therapies of organ fibrosis in the future.