Off-white crystalline powder
8-acetylshanzhiside methyl ester/acetylbarlerin/ipolamiidoside/8-O-Acetyl shanzhiside methyl ester/UmbrosideCyclopenta[c]pyran-4-carboxylic acid, 7-(acetyloxy)-1-(β-D-glucopyranosyloxy)-1,4a,5,6,7,7a-hexahydro-5-hydroxy-7-methyl-, methyl ester, (1S,4aS,5R,7S,7aS)-/8-O-acetylshanziside/Methyl (1S,4aS,5R,7S,7aS)-7-acetoxy-1-(β-D-glucopyranosyloxy)-5-hydroxy-7-methyl-1,4a,5,6,7,7a-hexahydrocyclopenta[c]pyran-4-carboxylate/Ac-Shanz-ME/Barlerin/O-Acetyl Shanzhiside Methyl Ester, 8-
634.2±55.0 °C at 760 mmHg
HS Code Reference
Personal Projective Equipment
For Reference Standard and R&D, Not for Human Use Directly.
provides coniferyl ferulate(CAS#:57420-46-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
Inflammatory activation plays a vital role in the pathophysiological mechanisms of stroke and diabetes mellitus (DM), exerts the deleterious effects on the progression of the brain and leads to vascular damage in diabetic stroke. The objectives of this study were to investigate the effects of 8-O-acetyl shanzhiside methylester (ND01) on tumour necrosis factor-α (TNF-α)-stimulated SH-SY5Y cell line in vitro and the experimental ischaemic diabetic stroke model in vivo. TNF-α-stimulated SH-SY5Y cells were pre-incubated with ND01, then analysed protein expression. For in vivo experiment, the diabetic rats were subjected to middle cerebral artery occlusion (MCAO) for 30 min. followed by reperfusion for 23 hr. Treatment of SH-SY5Y cells with ND01 blocked TNF-α-induced nuclear transcription factor κB (NF-κB) activation and decreased high-mobility group box-1 (HMGB-1) expression. ND01 40 mg/kg demonstrated significant neuroprotective effect even after delayed administration at 4 hr after I/R. ND01 40 mg/kg attenuated the histopathological damage, decreased brain swelling, inhibited NF-κB activation and reduced HMGB-1 expression in ischaemic brain tissue. These data show that ND01 protects diabetic brain against I/R injury with a favourable therapeutic time-window by alleviating diabetic cerebral I/R injury and attenuating blood-brain barrier (BBB) breakdown, and its protective effects may involve HMGB-1 and NF-κB signalling pathway.
© 2014 Nordic Association for the Publication of BCPT (former Nordic Pharmacological Society).
8-O-acetyl shanzhiside methylester attenuates cerebral ischaemia/reperfusion injury through an anti-inflammatory mechanism in diabetic rats.
Zhang L1, Kan ZC, Zhang XL, Fang H, Jiang WL.
We investigated whether 8-O-acetyl shanzhiside methylester (ND01) regulates angiogenesis and thereby improves functional outcome after stroke. Adult male rats were subjected to 1 hr of middle cerebral artery occlusion (MCAO) and reperfusion, and treated with or without different doses (5 and 10 mg/kg) of ND01, starting 24 hr after ischaemia and reperfusion (I/R) and by intravenous injection daily for 14 days. Neurological functional tests were performed and cerebral Evans blue extravasation was measured. Angiogenesis and angiogenic factor expression were measured by immunohistochemistry and Western blot, respectively. The results indicated that ND01 significantly promoted angiogenesis in the ischaemic brain and improved functional outcome after stroke. ND01 also significantly increased vascularization compared with vehicle treatment. ND01 increased the expression of VEGF, Ang1, phosphorylation of Tie2 and Akt VEGF. The Ang1/Tie2 axis and Akt pathways appear to mediate ND01-induced angiogenesis.
© 2010 The Authors. Basic & Clinical Pharmacology & Toxicology © 2010 Nordic Pharmacological Society.
Effect of 8-O-acetyl shanzhiside methylester increases angiogenesis and improves functional recovery after stroke.
Jiang WL1, Zhang SP, Zhu HB, Hou J.
8-O-acetyl shanzhiside methylester (ND01), an iridoid glucoside compound, was isolated from the leaves of Lamiophlomis rotata (Benth.) Kudo. The present study elucidated the effects of ND01 on the cultured rat cortical neuron injury induced by oxygen-glucose deprivation. The results showed that ND01 treatment obviously attenuated apoptosis and ameliorated mitochondrial energy metabolism in rat cortical neurons by increasing cell survival rate, mitochondrial respiratory enzyme activities, mitochondrial respiratory control ratio and adenosine triphosphate (ATP) content, and by attenuating lactate dehydrogenase (LDH) leakage, intracellular Ca(2+) level and caspase-3 activity in a concentration-dependent manner. These findings indicated that ND01 has potential against cerebral ischemic injury, and its protective effect on oxygen-glucose deprivation-induced injury might be due to the suppression of intracellular Ca(2+) elevation and caspase-3 activity, and improvement of mitochondrial energy metabolism.
Copyright (c) 2009 Elsevier B.V. All rights reserved.
8-O-acetyl shanzhiside methylester attenuates apoptosis and ameliorates mitochondrial energy metabolism in rat cortical neurons exposed to oxygen-glucose deprivation.
Jiang WL1, Fu FH, Zheng SG, Zhang DL, Zhu HB, Jian-Hou.
2010 Mar 10