Trillium tschonoskii Maxim/Dioscorea spp., Yucca spp., Trillium terrestris, Trillium kamtschaticum, Trillium erectum, Trigonella foenum-graecum and Paris polyphylla
Diosgenin 3-b-D-glucoside/β-D-Glucopyranoside, (3β,25R)-spirost-5-en-3-yl/Diosgenin 3-O-b-D-glucopyranoside/PolyphyllinA/Diosgenin b-D-glucoside/Polyphyllin A/Funkioside A/Diosgenin 3-glucoside/Collettinside I/Melongoside B/Diosgenin glucoside/(25R)-3β-(β-D-Glucopyranosyloxy)spirost-5-ene/(25R)-3b-(b-D-Glucopyranosyloxy)spirost-5-ene/Disogluside/Prosapogenin D'3/Lilioglycoside A/Alliumoside A/Polygonatoside A/Trillin/(3β,25R)-Spirost-5-en-3-yl β-D-glucopyranoside/Collettiside I
Diosgenin glucoside, a saponin compound extracted from Tritulus terrestris L., provides neuroprotection by regulating microglial M1 polarization. Diosgenin glucoside protects against spinal cord injury by regulating autophagy and alleviating apoptosis .
Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.
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Spinal cord injury (SCI) is a severe traumatic lesion of central nervous system (CNS) with only a limited number of restorative therapeutic options. Diosgenin glucoside (DG), a major bioactive ingredient of Trillium tschonoskii Max., possesses neuroprotective effects through its antioxidant and anti-apoptotic functions. In this study, we investigated the therapeutic benefit and underlying mechanisms of DG treatment in SCI. We found that in Sprague-Dawley rats with traumatic SCI, the expressions of autophagy marker Light Chain 3 (LC3) and Beclin1 were decreased with concomitant accumulation of autophagy substrate protein p62 and ubiquitinated proteins, indicating an impaired autophagic activity. DG treatment, however, significantly attenuated p62 expression and upregulated the Rheb/mTOR signaling pathway (evidenced as Ras homolog enriched in brain) due to the downregulation of miR-155-3p. We also observed significantly less tissue injury and edema in the DG-treated group, leading to appreciable functional recovery compared to that of the control group. Overall, the observed neuroprotection afforded by DG treatment warrants further investigation on its therapeutic potential in SCI.
Rheb/mTOR signal pathway; apoptosis; autophagy; diosgenin glucoside; miR-155-3p; spinal cord injury
Diosgenin Glucoside Protects against Spinal Cord Injury by Regulating Autophagy and Alleviating Apoptosis.
Chen XB1,2, Wang ZL3, Yang QY4, Zhao FY5, Qin XL6, Tang XE7, Du JL8, Chen ZH9, Zhang K10, Huang FJ11.
2018 Aug 2
The selective suppression of inflammatory factors in activated microglia, rather than totally inhibiting their activation, might be an effective means of slowing the progression of certain neurodegenerative diseases. Diosgenin glucoside (Dios) is a saponin compound extracted from Tritulus terrestris L. We found that Dios suppressed the synthesis of molecules that promote inflammation (M1 markers, such as NO, IL-6, and TNF-α) in rat microglia and BV-2 cells induced with lipopolysaccharides (LPS). In contrast, Dios had no effects on the cellular production of anti-inflammatory factors (M2 markers, such as IL-10, IL-1Rα and CD206) in LPS and IL-4 treated microglia. Dios repressed IκB-α, ERK MAPK and p38 MAPK phosphorylation, but did not affect JNK in LPS-activated microglia. We also found that conditioned medium obtained from cultures of BV-2 cells incubated with Dios plus LPS was markedly less neurotoxic than conditioned medium obtained from cultures of BV-2 cells incubated with LPS alone. In conclusion, this study demonstrated that Dios can selectively suppress the production/expression of pro-inflammatory M1 markers by activated microglia, without affecting M2 markers, and might provide neuroprotection by regulating microglial M1 polarization. Our results suggest that Dios can be used in treatment of various neuroinflammatory diseases mediated by microglia.
Copyright © 2017. Published by Elsevier B.V.
Diosgenin glucoside; Inflammation; Microglia; Neuroprotection
Diosgenin glucoside provides neuroprotection by regulating microglial M1 polarization.
Wang S1, Wang F2, Yang H1, Li R2, Guo H2, Hu L3.
The predominantly beta-anomer of diosgenin glucoside (DG) was synthesized and its effects on cholesterol homeostasis were tested in monkeys. Cynomolgus macaques (Macaca fascicularis) were fed, during two 3-week periods, a semipurified diet with 0.1% cholesterol and a similar ration containing 1% DG, respectively. A Chow diet was given for 5 weeks between the experimental periods. Cholesterol and bile acid balance were analyzed during the last week of each semipurified diet. Diosgenin glucoside reduced cholesterolemia from 292 mg/dl to 172 mg/dl, decreased intestinal absorption of exogenous cholesterol from 62.4% to 26.0%, and increased secretion of endogenous cholesterol from -0.8 to 93.5 mg/day. The fecal excretion of neutral steroids rose from 40.7 to 157.3 mg/day; that of bile acids changed, nonsignificantly, from 23.1 to 16.0 mg/day. The cholesterol balance was -44 mg/day in the control period, and 88 mg/day in the DG-fed animals. No toxic signs were observed. Thus, when long-term studies demonstrate that the glucoside is well tolerated, DG and other synthetic glycosides with similar activities may be of use in the management of hypercholesterolemia and atherosclerosis.
Effects of synthetic glycosides on steroid balance in Macaca fascicularis.
Malinow MR, Elliott WH, McLaughlin P, Upson B.