Table 4 Related effects of ginsenoside in attenuating adverse reactions induced by chemical antitumor drugs
Ginsenoside type | Anti-breast cancer activity | Cell line | In vivo/in vitro | Drugs that cause adverse reactions | Signaling pathway/target spot | Refs. |
|---|---|---|---|---|---|---|
Rg2 | Reducing cardiomyocyte apoptosis induced by trastuzumab therapy | / | In Vivo | Trastuzumab | caspase-3, caspase-9, Bax | [167] |
Rg2 | Promote the protective autophagy of myocardial cells and avoid the apoptosis of myocardial cells caused by trastuzumab therapy | Human primary HCMs | In Vitro | Trastuzumab | p-Akt, p-mTOR, beclin 1, LC3, ATG5 | [168] |
Rh2 | Cardiotoxicity is reduced by inhibiting cardiac histopathological changes, apoptosis and necrosis, and consequent inflammation. Pathological remodeling is attenuated by reducing fibroblast to myofibroblast transformation (FMT) and endothelial-mesenchymal transformation (EndMT). It can promote the senescence of myofibroblasts and reverse the differentiation of myofibroblasts established in EndMT to alleviate fibrosis | MDA-MB-231, HUVEC | In Vivo | Doxorubicin | caspase-3, caspase-7, caspase-9, TNF-α, IL-6, IL-1β, CD31, CD206, fα-SMA, Vimentin, Smad2, Smad3 | [169] |
Rg1 | Promote that specific combination of doxorubicin and tumor cells and avoid the apoptosis of myocardial cells induced by doxorubicin | / | In Vivo | Doxorubicin | ROS, p53, caspase-3 | [170] |
Panaxatriol | Reversing paclitaxel resistance | MDA-MB-231, SUM159 | In Vivo | Paclitaxel | RAK1/NF-κB and ERK signaling pathways, S100A7/9, inflammatory factors (IL6, IL8, CXCL1, CCL2), cancer stem cell-related (OCT4, SOX2, NANOG, ALDH1, CD44) | [49] |