A ginsenoside found in Panax ginseng and Panax japonicus var. major that is (20S)-ginsenoside Rg3 in which the hydroxy group at position 20 has been converted to its β-D-glucopyranoside.
InChI=1S/C48H82O18/c1-21(2)15-22(3)17-48(8,66-43-40(60)37(57)34(54)28(19-50)62-43)24-11-13-47(7)23-9-10-30-45(4,5)31(12-14-46(30,6)25(23)16-26(52)32(24)47)64-44-41(38(58)35(55)29(20-51)63-44)65-42-39(59)36(56)33(53)27(18-49)61-42/h15,22-44,49-60H,9-14,16-20H2,1-8H3/t22?,23?,24-,25?,26-,27+,28+,29+,30?,31?,32+,33+,34+,35+,36-,37-,38-,39+,40+,41+,42-,43-,44-,46+,47+,48-/m0/s1
Ginsenoside Rd (Rd), a saponin isolated from the roots of panax notoginseng, Rd has immunological adjuvant activity, and elicits a Th1 and Th2 immune response by regulating production and gene expression of Th1 cytokines and Th2 cytokines.[1]
Ginsenoside-Rd could play a crucial role in enhancing the defence system to counteract the aging process, through regulation of the GSH/GSSG redox status, decreasing in the superoxide dismutase (SOD) and catalase activity in old SAM.[2]
Ginsenoside-Rd treatment shows attenuation of hypertensive cerebrovascular remodeling, the underlying mechanism might be associated with inhibitory effects of ginsenoside-Rd on voltage-independent Ca 2+ entry and BAVSMC proliferation, but not with VDCC-mediated Ca 2+ entry.[3]
Ginsenoside Rd, a -type steroid extracted from , has exhibited an encouraging neuroprotective efficacy in both laboratory and clinical studies, could be as a neuroprotective agent for acute .[4]
Ginsenoside Rd can enhance the proliferation but not affect the differentiation of neural stem cells in vivo and in vitro.[5]
Ginsenoside Rd prevents glutamate-induced apoptosis in rat cortical neurons and may be the potential of voltage-independent Cachannel blockers as new neuroprotective drugs for the prevention of neuronal apoptosis and death induced by cerebral ischaemia.[6]
English website: Ginsenoside Rd
Japanese website: Ginsenoside Rd
Chinese website: Ginsenoside Rd
[1] Yang Z, Chen A, Sun H, et al. Vaccine, 2007, 25(1):161-9.
[2] Takako Y, Akiko S, Ju C E. J Pharma Pharmacol, 2004, 56(1):107-13.
[3] Cai B X, Li X Y, Chen J H, et al. Eur J Pharmacol, 2009, 606(1–3):142-9.
[4] Ye R, Gang Z, Liu X. Expert Rev Neuroth, 2013, 13(6):603-13.
[5] Lin T, Liu Y, Shi M, et al. J Ethnopharmacol, 2012, 142(3):754–61.
[6] Li X Y, Liang J, Tang Y B, et al. Clin Exp Pharmacol P , 2010, 37(2):199–204.
[7] Qin H Y, Suo Z R, Wei Y Q. Journal of Southwest University of Science & Technology, 2013, 28(02):92-94.
