Ginsenoside Rh2 reverses cyclophosphamide‐induced immune deficiency by regulating fatty acid metabolism. Issue 5 (18th June 2019)

• Record Type: Journal Article
• Authors: Qian, Ying; Huang, Rongrong; Li, Senlin; Xie, Rui; Qian, Bei; Zhang, Zijun; Li, Lei; Wang, Baotian; Tian, Cheng; Yang, Jian; Xiang, Ming
• Is Part Of: Journal of leukocyte biology. Volume 106:Issue 5(2019)
• Page Start: 1089
• Page End: 1100
• Publication Date: 2019-06-18
• Subjects: ginsenoside Rh2 -- immune deficiency -- metabolism regulation -- synergistic treatment; Leucocytes -- Periodicals; Reticulo-endothelial system -- Periodicals; 571.96
• DOI: 10.1002/JLB.2A0419-117R
• Languages: English
• ISSNs: 0741-5400

Abstract

Abstract: Ginsenoside Rh2 (G‐Rh2) has well‐established potent antitumor activity; yet, the effects of G‐Rh2 on immune and metabolism regulation in cancer treatment, especially non‐small cell lung cancer (NSCLC) remain unclear. We showed that G‐Rh2 had a synergistic antitumor effect with cyclophosphamide (CY) on mice with NSCLC, and improved the immune deficiency caused by CY. Consistently, G‐Rh2 exhibited no inhibitory effect on tumor growth of T cells‐deficient nude mice. Furthermore, G‐Rh2 treatment triggered the oxidative decomposition of fatty acid (FA), suppressed FA synthesis, increased ketone level, and decreased glucocorticoid (CORT) secretion. G‐Rh2 significantly down‐regulated the expression of fatty acid synthase ( FASN ). Of note, in liver‐specific FASN knockout mice G‐Rh2 failed to show the same immune enhancement effects. Further mechanistic exploration revealed that G‐Rh2 suppressed the expression and nuclear translocation of sterol regulatory element binding protein 1 (SREBP‐1 ), and disturbed the SREBP‐1 – FASN interaction in vitro. Abstract : Ginsenoside Rh2 may enhance the anti‐tumor immunology by inhibiting the transcription regulation of SREBP‐1 on FASN to suppress FA synthesis, increase ketone level, and decrease CORT secretion.