Catalogue Number
BF-S3018
Analysis Method
HPLC,NMR,MS
Specification
98%
Storage
2-8°C
Molecular Weight
536.574
Appearance
White crystal
Botanical Source
Schisandra chinensis
Structure Type
Lignanoids
Category
Standards;Natural Pytochemical;API
SMILES
CC1CC2=CC3=C(C(=C2C4=C(C(=C(C=C4C(C1(C)O)OC(=O)C5=CC=CC=C5)OC)OC)OC)OC)OCO3
Synonyms
Benzo[3',4']cycloocta[1',2':4,5]benzo[1,2-d][1,3]dioxole-5,6-diol, 5,6,7,8-tetrahydro-1,2,3,13-tetramethoxy-6,7-dimethyl-, 5-benzoate/(5S,6S,7S)-6-Hydroxy-1,2,3,13-tetramethoxy-6,7-dimethyl-5,6,7,8-tetrahydrobenzo[3',4']cycloocta[1',2':4,5]benzo[1,2-d][1,3]dioxol-5-yl benzoate/Benzo[3',4']cycloocta[1',2':4,5]benzo[1,2-d][1,3]dioxole-5,6-diol, 5,6,7,8-tetrahydro-1,2,3,13-tetramethoxy-6,7-dimethyl-, 5-benzoate, (5S,6S,7S)-/6-Hydroxy-1,2,3,13-tetramethoxy-6,7-dimethyl-5,6,7,8-tetrahydrobenzo[3',4']cycloocta[1',2':4,5]benzo[1,2-d][1,3]dioxol-5-yl benzoate/SCHISANTHERINGOMISIN/6-Hydroxy-1,2,3,13-tetramethoxy-6,7-dimethyl-5,6,7,8-tetrahydrobenzo[3,4]cycloocta[1,2-f][1,3]benzodioxol-5-yl benzoate/SchizantherinA/Schisantherin A
IUPAC Name
[(8S,9S,10S)-9-hydroxy-3,4,5,19-tetramethoxy-9,10-dimethyl-15,17-dioxatetracyclo[10.7.0.02,7.014,18]nonadeca-1(19),2,4,6,12,14(18)-hexaen-8-yl] benzoate
Density
1.3±0.1 g/cm3
Solubility
Methanol; Ethyl Acetate
Flash Point
218.9±25.0 °C
Boiling Point
675.6±55.0 °C at 760 mmHg
Melting Point
InChl
InChl Key
WGK Germany
RID/ADR
HS Code Reference
2932990000
Personal Projective Equipment
Correct Usage
For Reference Standard and R&D, Not for Human Use Directly.
Meta Tag
provides coniferyl ferulate(CAS#:58546-56-8) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate
MSDS
28690033
Toll-like receptor 4 (TLR4) and C5aR1 (CD88) have been recognized as potential therapeutic targets for the reduction of inflammation and secondary damage and improvement of outcome after ischemia and reperfusion (I/R). The inflammatory responses which induce cell apoptosis and necrosis after I/R brain injury lead to a limited process of neural repair. To further comprehend how these targets function in I/R state, we investigated the pathological changes and TLR4 and C5aR1 signaling pathways in vitro and in vivo models of I/R brain injury in this study. Meanwhile, we explored the roles of schisantherin A on I/R brain injury, and whether it exerted neuroprotective effects by regulating the TLR4 and C5aR1 signaling pathways or not. The results showed that schisantherin A significantly reduced the neuronal apoptosis induced by oxygen and glucose deprivation and reperfusion (OGD/R) injury in primary culture of rat cortical neurons. Also, schisantherin A alleviated neurological deficits, reduced infarct volume, attenuated oxidation stress, inflammation and apoptosis in ischemic parietal cortex of rats after middle cerebral artery occlusion and reperfusion (MCAO/R) injury. Moreover, the activated TLR4 and C5aR1 signaling pathways were inhibited by schisantherin A treatment. In conclusion, TLR4 and C5aR1 played a vital role during I/R brain injury in rats, and schisantherin A exhibited neuroprotective effects by TLR4 and C5aR1 signaling pathways. These findings also provided new insights that would aid in elucidating the effect of schisantherin A against cerebral I/R and support the development of schisantherin A as a potential treatment for ischemic stroke.
Copyright © 2017 Elsevier Inc. All rights reserved.
Apoptosis; C5aR1; Inflammation; Neuroprotection; Schisantherin A; TLR4
Schisantherin A attenuates ischemia/reperfusion-induced neuronal injury in rats via regulation of TLR4 and C5aR1 signaling pathways.
Shi YW1, Zhang XC1, Chen C1, Tang M1, Wang ZW2, Liang XM3, Ding F4, Wang CP5.
2017 Nov
24813830
Schisantherin A (STA) is a main bioactive lignan isolated from Schisandra chinensis (Turcz.) Baill., which has been widely used as a tonic in traditional Chinese medicine for many years. Lots of studies have reported that STA exhibited anti-inflammatory and antioxidant effects. This paper was designed to investigate the effects of STA on cognitive function and neurodegeneration in the mouse control of Alzheimer’s disease (AD) induced by Aβ1-42. It was found that successive intracerebroventricular (ICV) administration of STA (0.01 and 0.1mg/kg) for 5days significantly attenuated Aβ1-42-induced learning and memory impairment as measured by the Y-maze test, shuttle-box test and Morris water maze test. Furthermore, STA at a dose of 0.1mg/kg restored the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) as well as the levels of Aβ1-42, malondialdehyde (MDA) and glutathione (GSH) to some extent in the hippocampus and cerebral cortex. It also noticeably improved the histopathological changes in the hippocampus. The results suggested that STA might protect against cognitive deficits, oxidative stress and neurodegeneration induced by Aβ1-42, and serve as a potential agent in treatment of AD.
Copyright © 2014 Elsevier Inc. All rights reserved
Alzheimer's disease; Aβ(1-42); Cognition enhancing activity; Histopathological changes; Schisantherin A; Successive intracerebroventricular
Schisantherin A recovers Aβ-induced neurodegeneration with cognitive decline in mice.
Li X1, Zhao X1, Xu X1, Mao X1, Liu Z1, Li H1, Guo L1, Bi K2, Jia Y3.
2014 Jun 10
25934514
ETHNOPHARMACOLOGICAL RELEVANCE:
The fruit of Schisandra chinensis (Turcz.) Baill, has been traditionally used in management of liver diseases and ageing associated neurodegeneration. The bioactive compound from this medicinal plant would be valuable for its potential use in prevention and treatment of Parkinson׳s disease.
AIM OF THE STUDY:
The overall objective of the present study was to understand the neuroprotective effect of schisantherin A, a dibenzocyclooctadiene lignan from the fruit of S. chinensis (Turcz.) Baill, and to elucidate its underlying mechanism of action.
MATERIAL AND METHODS:
This study investigated the protective effect of schisantherin A against selective dopaminergic neurotoxin 6-hydroxydopamine (6-OHDA)-induced neural damage in human neuroblastoma SH-SY5Y cells and zebrafish models. Oxidative stress and related signaling pathways underlying the neuroprotective effect were determined by multiple biochemical assays and Western blot.
RESULTS:
Pretreatment with schisantherin A offered neuroprotection against 6-OHDA-induced SH-SY5Y cytotoxicity. Moreover, schisantherin A could prevent 6-OHDA-stimulated dopaminergic neuron loss in zebrafish. Our mechanistic study showed that schisantherin A can regulate intracellular ROS accumulation, and inhibit NO overproduction by down-regulating the over-expression of iNOS in 6-OHDA treated SH-SY5Y cells. Schisantherin A also protects against 6-OHDA-mediated activation of MAPKs, PI3K/Akt and GSK3β.
CONCLUSION:
These findings demonstrate that schisantherin A may have potential therapeutic value for neurodegenerative diseases associated with abnormal oxidative stress such as Parkinson׳s disease.
Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.
6-hydroxydopamine (6-OHDA); Oxidative stress; Parkinson׳s disease; Schisantherin A
Schisantherin A protects against 6-OHDA-induced dopaminergic neuron damage in zebrafish and cytotoxicity in SH-SY5Y cells through the ROS/NO and AKT/GSK3β pathways.
Zhang LQ1, Sa F1, Chong CM1, Wang Y1, Zhou ZY1, Chang RC2, Chan SW3, Hoi PM1, Yuen Lee SM4.
2015 Jul 21
