8-O-Acetylshanzhiside methyl ester
8-O-Acetylshanzhiside methyl ester(ND01) has potential against cerebral ischemic injury and experimental myocardial ischemia injury, it can increase angiogenesis and improve functional recovery after stroke. ND01 protects diabetic brain against I/R injury 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.
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Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to
24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
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Eur J Pharm Sci. 2012 Aug 30;47(1):124-30.
Cardioprotection with 8-O-acetylshanzhiside methylester on experimental myocardial ischemia injury.[Pubmed:
22677812 ]
8-O-Acetylshanzhiside methyl ester (ND01) was isolated from the leaves of Lamiophlomis rotata (Benth.) Kudo. In this study, we investigated the anti-myocardial ischemia and reperfusion (I/R) injury effects of ND01 in vivo and elucidated the potential mechanism in vitro.
METHODS AND RESULTS:
The results indicated that ND01 significantly attenuated hypoxia-induced cytotoxicity in a concentration-dependent manner in H9c2 cells. Treatment of H9c2 cells with ND01 9 μM blocked TNF-α-induced nuclear factor kappaB (NF-κB) phosphorylation by blocking High-mobility group box1 (HMGB1) expression. Treatment of rats with ND01 10mg/kg, (i.v.) protected the animals from myocardial I/R injury as indicated by a decrease in infarct volume, improvement in hemodynamics and reduction of myocardial damage severity. Treatment with ND01 also lowered serum levels of pro-inflammatory factors and reduced High mobility group box-1 protein (HMGB1) and phosphorylated NF-κB expression in ischemic myocardial tissue. Additionally, continuous i.v. of ND01 14 days attenuated cardiac remodeling.
CONCLUSIONS:
These protective effects suggested that ND01 might be due to block of myocardial inflammatory cascades through an HMGB1-dependent NF-κB signaling pathway.
Basic Clin Pharmacol Toxicol. 2011 Jan;108(1):21-7.
Effect of 8-O-acetyl shanzhiside methylester increases angiogenesis and improves functional recovery after stroke.[Pubmed:
20735376]
We investigated whether 8-O-Acetylshanzhiside methyl ester (ND01) regulates angiogenesis and thereby improves functional outcome after stroke.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.
J Ethnopharmacol . 2016 Jul 1;187:232-8.
A new anti-fibrinolytic hemostatic compound 8-O-acetyl shanzhiside methylester extracted from Lamiophlomis rotata[Pubmed:
27085939]
Abstract
Background: Fibrinolysis prevents blood clots from growing and becoming problematic. Antifibrinolytics are used as inhibitors of fibrinolysis. Aprotinin was doubted after identification of major side effects, especially on kidney. Lysine analogues has their own defects and whether they are adequate substitutes for aprotinin is still under doubt. Lamiophlomis rotata (Benth.) Kudo. was previous found to have hemostatic activity. But the active compound in L. rotata and its hemostatic mechanism were unknown.
Objectives: To find the major hemostatic compound in L. rotata and identify its haemostasis mechanism.
Methods: Traumatic hemorrhage model and coagulant activity assays were monitored in mice and platelets in drug treatment group and control group. Hyperfibrinolysis model was established by intravenous administration of urokinase in mice. Capillary blood clotting time (CBCT), activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), fibrinogen and euglobulin clot lysis time (ECLT) were measured.
Results: The anti-fibrinolytic activity come from 8-O-Acetyl shanzhiside methylester (ASM) one of the highest iridoid glycosides contents in TIG extracted from L. rotata. ASM significantly (P<0.05) shorten CBCT and reduced blood loss volume in vivo, but did not influence mice APTT, PT or TT. In particular, it significantly prolonged ECLT in hyperfibrinolysis mice. It indicated that ASM could inhibit fibrinolysis. ASM was also effective in CBCT, traumatic bleeding volume and ECLT in hyperfibrinolysis mice model.
Conclusions: ASM was the major hemostatic compound in L. rotata. The haemostasis mechanism of ASM was achieved by anti-fibrinolytic activity. ASM was a new fibrinolysis inhibitor as iridoid glycoside compound.
Keywords: Antifibrinolytics; Bleeding volume; Hemostatics; Hyperfibrinolysis; Iridoid glycosides.
Eur J Pharmacol. 2010 Mar 10;629(1-3):20-4.
8-O-acetyl shanzhiside methylester attenuates apoptosis and ameliorates mitochondrial energy metabolism in rat cortical neurons exposed to oxygen-glucose deprivation.[Pubmed:
19961847]
8-O-Acetylshanzhiside methyl ester (ND01), an iridoid glucoside compound, was isolated from the leaves of Lamiophlomis rotata (Benth.) Kudo.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.
Basic Clin Pharmacol Toxicol. 2014 Dec;115(6):481-7.
8-O-acetyl shanzhiside methylester attenuates cerebral ischaemia/reperfusion injury through an anti-inflammatory mechanism in diabetic rats.[Pubmed:
24823762 ]
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-Acetylshanzhiside methyl ester (ND01) on tumour necrosis factor-α (TNF-α)-stimulated SH-SY5Y cell line in vitro and the experimental ischaemic diabetic stroke model in vivo.
METHODS AND RESULTS:
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.
CONCLUSIONS:
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.
