Panax ginseng and its ginsenosides: potential candidates for the prevention and treatment of chemotherapy-induced side effects

• Published in: Journal of ginseng research Vol. 45; no. 6; pp. 617 - 630
• Main Authors: Wan, Yan, Wang, Jing, Xu, Jin-feng, Tang, Fei, Chen, Lu, Tan, Yu-zhu, Rao, Chao-long, Ao, Hui, Peng, Cheng
• Format: Journal Article
• Language: English
• Published: Elsevier B.V 01.11.2021; 고려인삼학회; Elsevier
• Subjects: Chemotherapy; Ginsenosides; Mechanism; Pharmacological effects; Review; Side effects; 기타의약학; JNK; ALT; ADM; FBG; FRGE; MDA; Ginsenosides; NF-κB; PGLF; PI3K; GM-CSF; mTOR; CIA; AMO; IL; LSK; PGFR; MAPK; PGSD; KG-KH; RGE; Chemotherapy; Side effects; MEK; ARE; PGSM; RG; ROS; AMPK; CYP2E1; ERG; PGS; ERK; LLC-PK1; MKK4; PPD; SREBP-1; HSPCS; HO-1; Mechanism; Nrf2; PPT; PGRT; BMNC; AST; Pharmacological effects; HEI-OC1; DAC; CK; CP; NQO; wRG; TNF-α; CY; PG; FRG; 5-FU
• ISSN: 1226-8453; 2093-4947
• DOI: 10.1016/j.jgr.2021.03.001

Chemotherapy-induced side effects affect the quality of life and efficacy of treatment of cancer patients. Current approaches for treating the side effects of chemotherapy are poorly effective and may cause numerous harmful side effects. Therefore, developing new and effective drugs derived from natural non-toxic compounds for the treatment of chemotherapy-induced side effects is necessary. Experiments in vivo and in vitro indicate that Panax ginseng (PG) and its ginsenosides are undoubtedly non-toxic and effective options for the treatment of chemotherapy-induced side effects, such as nephrotoxicity, hepatotoxicity, cardiotoxicity, immunotoxicity, and hematopoietic inhibition. The mechanism focus on anti-oxidation, anti-inflammation, and anti-apoptosis, as well as the modulation of signaling pathways, such as nuclear factor erythroid-2 related factor 2 (Nrf2)/heme oxygenase-1 (HO-1), P62/keap1/Nrf2, c-jun N-terminal kinase (JNK)/P53/caspase 3, mitogen-activated protein kinase (MEK)/extracellular signal-regulated kinases (ERK), AMP-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR), mitogen-activated protein kinase kinase 4 (MKK4)/JNK, and phosphatidylinositol 3-kinase (PI3K)/AKT. Since a systemic review of the effect and mechanism of PG and its ginsenosides on chemotherapy-induced side effects has not yet been published, we provide a comprehensive summarization with this aim and shed light on the future research of PG. [Display omitted]