InChI=1S/C53H90O22/c1-23(2)10-9-14-53(8,75-47-43(67)39(63)37(61)29(72-47)22-69-45-41(65)34(58)26(57)21-68-45)24-11-16-52(7)33(24)25(56)18-31-50(5)15-13-32(49(3,4)30(50)12-17-51(31,52)6)73-48-44(40(64)36(60)28(20-55)71-48)74-46-42(66)38(62)35(59)27(19-54)70-46/h10,24-48,54-67H,9,11-22H2,1-8H3/t24-,25+,26-,27+,28+,29+,30-,31+,32-,33-,34-,35+,36+,37+,38-,39?,40-,41+,42+,43+,44+,45-,46-,47-,48-,50-,51+,52+,53-/m0/s1
Ginsenosides, which are active compounds found in ginseng (Panax ginseng), are used as antidiabetic treatments; ginsenoside Rb2 may inhibit palmitate-induced gluconeogenesis via AMPK-induced SHP by relieving ER stress, a cause of gluconeogenesis.[1]
Ginsenoside Rb2 is a inducer of the SOD1 gene, the SOD1 gene is greatly activated by ginsenoside Rb2 through transcription factor AP2 binding sites and its induction.[2]
The intra-tumoral or oral administration of ginsenoside-Rb2 causes a marked inhibition of both neovascularization and tumor growth,the inhibition of tumor-associated angiogenesis by ginsenoside-Rb2 may partly contribute to the inhibition of lung tumor metastasis.[3]
Ginsenoside-Rb2 has hypoglycemic activity in streptozotocin-diabetic rat, one of the mechanisms probably is the changes of glucokinase and glucose-6-phosphatase levels.
Ginsenoside-Rb2 has anti-oxidant activity, has hydroxyl radical scavenging activity changes by heat processing.[4]
Ginsenoside Rb2 can enhance the expression of the sterol regulated element binding protein (SREBP) mRNA whereas treatment with cholesterol and FBS led to a reduction in the abundance of this transcript, suggests that it might be a valuable component capable of lowering the levels of lipids.[5]
Ginsenoside-Rb2 is the most effective among ginsenosides from red ginseng to prevent the lethal infection of HVJ, so that this ginsenoside is a promising candidate as a mucosal immunoadjuvant to enhance antiviral activity.[6]
English website: Ginsenoside Rb2
Japanese website: Ginsenoside Rb2
Chinese website: Ginsenoside Rb2
[1] Lee K T, Jung T W, Lee H J, et al. Arch Pharm Res, 2011, 34(7):1201-8.
[2] Kim Y H, Park K H, Rho H M. J Biol Chem, 1996, 271(40):24539-43.
[3] Sato K, Mochizuki M, Saiki I, et al. Biol Pharm Bull, 1994, 17(5):635-9.
[4] Kang K S, Kim H Y, Baek S H, et al. Biol Pharm Bull, 2007, 30(4):724-8.
[5] Kim E J, Lee H I, Chung K J, et al. Bmb Rep, 2009, 42(4):194-9.
[6] Yin S, Wu H, Xu F, et al. Acta Acad Med Militaris Tertiae, 2010, 32(7):658-60.
[7] Yoo Y C, Lee J, Park S R, et al. J Ginseng Res, 2013, 37(1):80-6.
