Schisandrone
Schisandrone has strong activities of anti-oxidation, effectively scavenges hydroxyl radical and superoxide anion, and has protective effects on cells under active oxygen stress state. Schisandrone can significantly decrease phosphorylation levels of Tau protein at 396, 262 sites, and relieve neuronal injury, but the phosphorylation level does not reach a negative cell level; it can suppress the Aβ-induced oxidative stress and inflammatory reaction through influencing NF-κB signaling pathway, exerting its protective effect on Alzheimer disease.
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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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Journal of Clinical Rehabilitative Tissue Engineering Research,2009 ,13 (23) :4490-4.
Effects of schisandrone on Tau protein hyperphosphorylation in differentiation of neural stem cells from APP transgenic mice[Reference:
WebLink]
Schisandrone has strong activities of anti-oxidation, effectively scavenges hydroxyl radical and superoxide anion, and has protective effects on cells under active oxygen stress state. Neurofibrillary tangles in neurons is composed of abnormal phosphorylation Tau protein and positively correlated with severity of Alzheimer disease.
METHODS AND RESULTS:
To explore the effect of Schisandrone on tau protein phosphorylation in the process of differentiation of APP transgenic mouse neural stem cells into neural cells. Compared with the APP+ cell control group, cell fluorescence intensity became weak in the Schisandrone group. Phosphorylation levels of Tau[Ps262] and Tau[Ps396] were reduced, especially at Tau[Ps396] site. Phosphorylation levels of Tau[Ps262] and Tau[Ps396] were low in the APP- cell control group.
CONCLUSIONS:
In the process of differentiation of APP transgenic mouse neural stem cells, Schisandrone can significantly decrease phosphorylation levels of Tau protein at 396, 262 sites, and relieve neuronal injury, but the phosphorylation level does not reach a negative cell level.
Academic Journal of Second Military Medical University,2007,28 (12) :1351-5.
Schisandrone improves learning and memory abilities of Alzheimer-like rats and influences expression of NF-κB, iNOS in rat hippocampus[Reference:
WebLink]
To investigate the influence of Schisandrone on the learning and memory abilities of rats with Alzheimer-like disease and on the expression of NF-κB, iNOS in rat hippocampus, so as to study the prevention effect of Schisandrone on Alzheimer disease (AD).
METHODS AND RESULTS:
Totally 30 male SD rats were evenly randomized into 3 groups: blank control group, AD model group and Schisandrone intervention group. The AD animal model was established by stereotactic injection of Aβ25-35 into lateral cerebral ventricle of rats; the rats in Schisandrone intervention group were administrated with Schisandrone. The learning and memory abilities of animals were determined by Morris water maze; the expression of NF-κB, iNOS in the hippocampus was detected by immunohistochemistry. The learning and memory abilities of rats in the Schisandrone intervention group were significantly improved compared with those in the AD model group (P<0.05). The expression of NF-κB and iNOS in the hippocampus was significantly decreased in the Schisandrone group than in the AD model group(P<0.05). The expression of NF-κB and iNOS in the hippocampus was positively correlated with each other. The correlation coefficients for the blank control,AD model and Schisandrone intervention groups were 0.639,0.656 and 0.682, respectively(all P<0.05).
CONCLUSIONS:
Schisandrone can suppress the Aβ-induced oxidative stress and inflammatory reaction through influencing NF-κB signaling pathway, exerting its protective effect on AD.
