Difference between revisions of "Berberine"

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:''Berberine’s main mechanism is partly responsible for its anti-diabetic and anti-inflammatory effects. Berberine is able to activate an enzyme called Adenosine Monophosphate-Activated Protein Kinase (AMPK) while inhibiting Protein-Tyrosine Phosphatase 1B (PTP1B).''
 
:''Berberine’s main mechanism is partly responsible for its anti-diabetic and anti-inflammatory effects. Berberine is able to activate an enzyme called Adenosine Monophosphate-Activated Protein Kinase (AMPK) while inhibiting Protein-Tyrosine Phosphatase 1B (PTP1B).''
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== Effect of berberine on ALS ==
  
 
In rat cerebral cortex, berberine inhibits synaptosomal glutamate release. [1]
 
In rat cerebral cortex, berberine inhibits synaptosomal glutamate release. [1]
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== Discussion threads on the ALSTDI forum ==
 
== Discussion threads on the ALSTDI forum ==
  
 
[http://www.alstdi.org/forum/yaf_postst48627_berberine.aspx Berberine]
 
[http://www.alstdi.org/forum/yaf_postst48627_berberine.aspx Berberine]
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== Regulated pathways ==
  
  

Revision as of 20:13, 30 September 2015

Information on nutritional supplements people with ALS have been taking

Wikipedia page

examine.com summarizes:

Berberine is an alkaloid extracted from various plants used in Traditional Chinese Medicine.
Berberine is supplemented for its anti-inflammatory and anti-diabetic effects. It can also improve intestinal health and lower cholesterol. Berberine is able to reduce glucose production in the liver. Human and animal research demonstrates that 1500mg of berberine, taken in three doses of 500mg each, is equally effective as taking 1500mg of metformin or 4mg glibenclamide, two pharmaceuticals for treating type II diabetes. Effectiveness was measured by how well the drugs reduced biomarkers of type II diabetes.
Berberine may also synergize with anti-depressant medication and help with body fat loss. Both of these benefits need additional evidence behind them before berberine can be recommended specifically for these reasons.
Berberine’s main mechanism is partly responsible for its anti-diabetic and anti-inflammatory effects. Berberine is able to activate an enzyme called Adenosine Monophosphate-Activated Protein Kinase (AMPK) while inhibiting Protein-Tyrosine Phosphatase 1B (PTP1B).


Effect of berberine on ALS

In rat cerebral cortex, berberine inhibits synaptosomal glutamate release. [1]

Discussion threads on the ALSTDI forum

Berberine


Regulated pathways

References

[1] <bibtex> @article{Lin2013, abstract = {Berberine, an isoquinoline plant alkaloid, protects neurons against neurotoxicity. An excessive release of glutamate is considered to be one of the molecular mechanisms of neuronal damage in several neurological diseases. In this study, we investigated whether berberine could affect endogenous glutamate release in nerve terminals of rat cerebral cortex (synaptosomes) and explored the possible mechanism. Berberine inhibited the release of glutamate evoked by the K(+) channel blocker 4-aminopyridine (4-AP), and this phenomenon was prevented by the chelating extracellular Ca(2+) ions and the vesicular transporter inhibitor bafilomycin A1, but was insensitive to the glutamate transporter inhibitor DL-threo-beta-benzyl-oxyaspartate. Inhibition of glutamate release by berberine was not due to it decreasing synaptosomal excitability, because berberine did not alter 4-AP-mediated depolarization. The inhibitory effect of berberine on glutamate release was associated with a reduction in the depolarization-induced increase in cytosolic free Ca(2+) concentration. Involvement of the Cav2.1 (P/Q-type) channels in the berberine action was confirmed by blockade of the berberine-mediated inhibition of glutamate release by the Cav2.1 (P/Q-type) channel blocker $\omega$-agatoxin IVA. In addition, the inhibitory effect of berberine on evoked glutamate release was prevented by the mitogen-activated/extracellular signal-regulated kinase kinase (MEK) inhibitors. Berberine decreased the 4-AP-induced phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and synapsin I, the main presynaptic target of ERK; this decrease was also blocked by the MEK inhibition. Moreover, the inhibitory effect of berberine on evoked glutamate release was prevented in nerve terminals from mice lacking synapsin I. Together, these results indicated that berberine inhibits glutamate release from rats cortical synaptosomes, through the suppression of presynaptic Cav2.1 channels and ERK/synapsin I signaling cascade. This finding may provide further understanding of the mode of berberine action in the brain and highlights the therapeutic potential of this compound in the treatment of a wide range of neurological disorders.}, author = {Lin, Tzu-Yu and Lin, Yu-Wan and Lu, Cheng-Wei and Huang, Shu-Kuei and Wang, Su-Jane}, doi = {10.1371/journal.pone.0067215}, editor = {Woodhall, Gavin}, file = {:C$\backslash$:/Users/riku/AppData/Local/Mendeley Ltd./Mendeley Desktop/Downloaded/Lin et al. - 2013 - Berberine Inhibits the Release of Glutamate in Nerve Terminals from Rat Cerebral Cortex(2).pdf:pdf}, issn = {1932-6203}, journal = {PLoS ONE}, mendeley-groups = {berberine}, month = jun, number = {6}, pages = {e67215}, pmid = {23840629}, title = Template:Berberine Inhibits the Release of Glutamate in Nerve Terminals from Rat Cerebral Cortex, url = {http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=3686739\&tool=pmcentrez\&rendertype=abstract}, volume = {8}, year = {2013} }

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