Cedrin
Cedrin has protective effects on PC12 cells against the neurotoxicity induced by amyloid β1-42, the protective effect is related to the inhibition of oxidative stress, improvement of mitochondrial dysfunction and suppression of apoptosis.
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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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The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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Nat Prod Res. 2017 Jun 29:1-4.
Cedrin identified from Cedrus deodara (Roxb.) G. Don protects PC12 cells against neurotoxicity induced by Aβ1-42.[Pubmed:
28658984 ]
Alzheimer's disease is a severe neurodegenerative disease affecting elder worldwide and closely related to the neurotoxicity induced by amyloid β.
METHODS AND RESULTS:
To find efficient therapeutics, we have investigated the protective effects of Cedrin from Cedrus deodara (Roxb.) G. Don on PC12 cells against the neurotoxicity induced by amyloid β1-42. The results have shown the viability of PC12 cells injured by amyloid β1-42 can be improved by Cedrin. Cedrin can reduce reacrive oxygen species overproduction, increase the activity of superoxide dismutase and decrease malondialdehyde content. Meanwhile, the loss of mitochondrial membrane potential and mitochondrial permeability transition pore opening in PC12 cells, and elevated Caspase-3 activity, downregulated Bcl-2 and upregulated Bax are meliorated.
CONCLUSIONS:
These results demonstrate the protective effect of Cedrin is related to the inhibition of oxidative stress, improvement of mitochondrial dysfunction and suppression of apoptosis. This investigation gives evidences for the application of Cedrin in practice and further investigation in vivo.
