Butylphthalide (Natural) - CAS 6066-49-5
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Not Intended for Therapeutic Use. For research use only.
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Butylphthalide is an anti-cerebral-ischemia drug, which is first isolated from the seeds of celery, showed efficacy in animal models of stroke. It alleviates oxidative stress caused by chronic cerebral ischemia, improves cholinergic function, and inhibits amyloid beta accumulation, thereby improving cerebral neuronal injury and cognitive deficits.
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3-n-Butylphthalide; 3-Butylphthalide
1.[Correlation Analysis Between Common Peaks of Angelica sinensis HPLC Fingerprint and Mineral Elements in Its Growing Soil].
Ding JX, Gu ZR, Wang YL, Zhang YY, Wang YP, Sun YJ. Zhong Yao Cai. 2015 Aug;38(8):1595-9.
OBJECTIVE: To investigate the correlation between common peaks of Angelica sinensis HPLC fingerprint and mineral elements in its growing soil.
2.Dl-3-n-butylphthalide-induced upregulation of antioxidant defense is involved in the enhancement of cross talk between CREB and Nrf2 in an Alzheimer's disease mouse model.
Wang CY1, Wang ZY2, Xie JW3, Wang T2, Wang X4, Xu Y5, Cai JH6. Neurobiol Aging. 2016 Feb;38:32-46. doi: 10.1016/j.neurobiolaging.2015.10.024. Epub 2015 Nov 2.
Synapse impairment in the Alzheimer's disease (AD) brain is an early event leading to cognitive dysfunction. Most oxidative stress localizes to the synapse, and synapse loss is the basis of cognitive decline in AD. Dl-3-n-butylphthalide (Dl-NBP), a small molecule compound has been shown to ameliorate oxidative stress. We evaluated the effects of a 5-month oral delivery with Dl-NBP on oxidative stress and cognitive function in APP/PS1 transgenic mice. Dl-NBP treatment reduced oxidative stress in the APP/PS1 mouse brain and alleviated learning and memory deficits. Dl-NBP supplementation meliorated synaptic plasticity, diminished soluble amyloid beta and amyloid beta oligomer in the APP/PS1 mouse brain. Dl-NBP administration caused an increase of cyclic adenosine monophosphate-response element binding protein (CREB)-binding protein (CBP)-associated Ser133-phosphorylated CREB (p-CREB) protein. Chromatin immunoprecipitation analysis revealed that Dl-NBP increased the recruitment of CBP to the promoters of best-characterized genes downstream of nuclear factor erythroid 2-related factor 2, nicotinamide adenine dinucleotide phosphate (NADPH) quinone oxidoreductase 1, and γ-glutamylcysteine synthetase modifier subunit.
3.Synthesis and biological evaluation of n-butylphthalide derivatives as anti-platelet aggregation agents.
Chen M1,2, Liu Q3, Tan M4, Wen S5, Pi R3, Lin D1,2. Nat Prod Res. 2016 Feb 15:1-4. [Epub ahead of print]
New analogues of n-butylphthalide (NBP) bearing various lengths of alkyl and different substitution at the two-position of phthalide were designed and synthesised. Preliminary evaluation and prediction of ACD LogP software indicate that the derivatives display significant improvement in water solubility than NBP does. Further biological analysis showed that NBP analogues specifically inhibit platelet aggregation induced by arachidonic acid but have no effect on that induced by adenosine 5-diphosphate. Especially compounds 1 and 3 were stronger than classical anti-platelet drug, aspirin, and equal potent with NBP, respectively. These findings provide an alternative approach to the development of NBP analogues with anti-platelet aggregation activity with good water solubility for the intervention of ischemic stroke.
4.Butylphthalide Suppresses Neuronal Cells Apoptosis and Inhibits JNK-Caspase3 Signaling Pathway After Brain Ischemia /Reperfusion in Rats.
Wen XR1,2, Tang M1,3, Qi DS1,4, Huang XJ5, Liu HZ1, Zhang F1, Wu J1, Wang YW5, Zhang XB5, Guo JQ6, Wang SL7, Liu Y1, Wang YL3, Song YJ8,9. Cell Mol Neurobiol. 2016 Mar 25. [Epub ahead of print]
Although Butylphthalide (BP) has protective effects that reduce ischemia-induced brain damage and neuronal cell death, little is known about the precise mechanisms occurring during cerebral ischemia/reperfusion (I/R). Therefore, the aim of this study was to investigate the neuroprotective mechanisms of BP against ischemic brain injury induced by cerebral I/R through inhibition of the c-Jun N-terminal kinase (JNK)-Caspase3 signaling pathway. BP in distilled non-genetically modified Soybean oil was administered intragastrically three times a day at a dosage of 15 mg/(kg day) beginning at 20 min after I/R in Sprague-Dawley rats. Immunohistochemical staining and Western blotting were performed to examine the expression of related proteins, and TUNEL-staining was used to detect the percentage of neuronal apoptosis in the hippocampal CA1 region. The results showed that BP could significantly protect neurons against cerebral I/R-induced damage.
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CAS 6066-49-5 Butylphthalide (Natural)

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