Special Price for Huperzine A Factory in Abu Dhabi


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Special Price for Huperzine A Factory in Abu Dhabi Detail:

[Latin Name]Huperzia serratum

[Source] Huperziceae whole herb from China

[Appearance]Brown to white

[Ingredient]Huperzine A

[Specification]Huperzine A 1% – 5%, HPLC

[Solubility] Soluble in chloroform, methanol, ethanol, slightly soluble in water

[Particle size] 80 Mesh

[Loss on drying] ≤5.0%

[Heavy Metal] ≤10PPM

[Pesticide residue] EC396-2005, USP 34, EP 8.0, FDA

[Storage] Store in cool & dry area, keep away from the direct light and heat.

[Shelf life] 24 Months

[Package] Packed in paper-drums and two plastic-bags inside.

Huperzine A111

[What is Huperzine A]

Huperzia is a type of moss that grows in China. It is related to club mosses (the Lycopodiaceae family) and is known to some botanists as Lycopodium serratum . The whole prepared moss was used traditionally. Modern herbal preparations use only the isolated alkaloid known as huperzine A. Huperzine A is an alkaloid found in huperzia that has been reported to prevent the breakdown of acetylcholine, an important substance needed by the nervous system to transmit information from cell to cell. Animal research has suggested that huperzine A’s ability to preserve acetylcholine may be greater than that of some prescription drugs. Loss of acetylcholine function is a primary feature of several disorders of brain function, including Alzheimer’s disease . Huperzine A may also have a protective effect on brain tissue, further increasing its theoretical potential for helping reduce symptoms of some brain disorders.

Huperzine A122211

[Function] Used in alternative medicine, huperzine A has been found to act as a cholinesterase inhibitor, a type of medicine used to prevent the breakdown of acetylcholine (a chemical essential to learning and memory).

Not only used as a treatment for Alzheimer’s disease, huperzine A is also said to enhance learning and memory and to protect against age-related cognitive decline.

In addition, huperzine A is sometimes used to boost energy, increase alertness, and aid in the treatment of myasthenia gravis (an autoimmune disorder that affects the muscles).


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    Title: Cyanidin-3-O-glucoside ameliorates lipid and glucose accumulation in C57BL/6J mice via activation of PPAR-α and AMPK?
    3rdInternational Conference and Exhibition on Nutrition & Food Sciences
    September 23-25, 2014 Valencia , Spain

    OMICS International: https://conferenceseries.com/
    Pharmaceutical Conferences: https://pharmaceuticalconferences.com
    Global OMICS open access Journals: https://omicsonline.org
    Global Medical Conferences: https://conferenceseries.com
    Global Cancer Conferences: https://cancersummit.org
    Global Diabetes Conferences: https://diabetesexpo.com
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    Abstract
    Cyanidin-3-O-glucoside (C3G) is an anthocyanidin abundant in fruits and vegetables that exhibits potent activities in energy metabolism; however, molecular target(s) and the mode of actions of C3G have been elusive. Surface plasmon resonance and time-resolved fluorescence resonance energy transfer analyses revealed that C3G directly interacted with PPARα ligand-binding domain, thus the C3G induced hepatic fatty acid oxidation and ketogenesis regulating PPARα responsive genes. C3G also bound directly to the α1 subunit of AMPK in cell-free kinase assay, phosphorylated ACC1, decreased hepatic malonyl- CoA concentration, thus reduced hepatic fatty acid synthesis. In high-fat-diet fed C57BL/6J mice orally administrated with C3G for 8 weeks, hepatic and plasma triglycerides were significantly reduced due to the combined effects of PPARα and AMPK activation. Insulin resistance and glucose tolerance were significantly improved with reduction in hepatic gluconeogenesis in C3G mice compared with those of controls. The AMPK activation by C3G led to the phosphorylation inhibition of FoxO1 and CREB to suppress the expressions of key genes in hepatic gluconeogenesis. Body fat accumulation was reduced in C3G fed mice with induction of thermogenic gene expressions in brown adipocytes and energy expenditure was significantly increased in mice fed C3G. Hepatic autophagy pathway was significantly activated in C3G livers, via activation AMPK-mTORsignaling axis and PPARα activation. Autophagy activation may contribute to lowering lipid accumulation in the liver. Collectively, these demonstrate that C3G in diet has profound metabolic roles in regulating lipid metabolism and insulin resistance via activation of both PPARα and AMPK.

    Biography

    YaoyaoJia earned her Degree of Doctor of Philosophy from Food Science and Technology Department of Biotechnology Graduate School of Korea University. Her research is mainly focus on effects of natural compounds in cellular lipid metabolism and regulation of PPAR activity.

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