人々の “健康促進” のために!

人々の “健康促進” のために!
2015年春、沖縄の琉球大学キャンパス内 (産学共同研究棟) に立ち上げた “PAK研究センター” の発足メンバー(左から4人目が、所長の多和田真吉名誉教授)
For detail, click the above image.

2009年9月2日水曜日

Propolis is Good for Diabetes, Why?

Propolis in general, whether it is based on CAPE or ARC (Artepillin C),
has been known to be useful for the treatment of diabetes (both types 1
and 2). However, it remained unclear for a while how propolis could reduce
the blood sugar levels. Well, in 2007, a Korean group led by Hyeon Soo Kim
at Korean University Medical School in Seoul found that CAPE activates the
kinase AMPK somehow, leading to the reduction of blood sugar level by activating
a glucose transporter called "GLUT-4". Then, I wonder why ARC-based propolis
such as Brazilian green propolis is also effective in reducing the blood
sugar levels. I postulate that ARC must be responsible for this anti-diabetic
action, because nothing else in this propolis is good for the treatment
of cancers, NF, TSC and several other PAK-dependent diseases.

What is the most common biological property shared between CAPE and ARC?
Both block selectively the oncogenic kinase PAK.

Interestingly, there are several other natural products that block the kinase
PAK as well as activate the kinase AMPK, as does CAPE: curcumin, berberine,
resveratrol (trans R3), salidroside, and triterpenoids from bitter melon,
Moreover, both PAK inactivation and AMPK activation lead to the same outcome,
activation of the tumor suppressor "FOXO" which is essential for both the
activation of Hsp16 gene and the longevity. So I would hypothesize that
these natural products activate AMPK most likely by inactivating PAK which
I think normally inactivates AMPK somehow, proposing a new unified formula:

anti-PAK drugs=AMPK activators=FOXO activators=Hsp16 activators= "elixirs"


In other words, the best (quickest and least expensive) in vivo drug screening
system to explore the anti-PAK drugs (=elixirs) would be to monitor the
GFP expression in C. elegans (strain CL2070) which carries the Hsp16-GFP
fusion gene, that is rapidly activated shortly after heat-shock treatment,
only if PAK is blocked.

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