chemrox - 28-1-2013 at 17:11
I ran across some very interesting information on liver fibrosis reversal through CB-1 antagonism to the endocannabinoid system. This is quite a
distance form my comfort level and education. I would like someone familiar with this kind of biochem to tutor me on the subject. Is a CB-1
endocannabinoid antagonist something that could be found or derived from Cannabis? Would a reasonable treatment for hepatic fibrosis be medical
marijuana? It seems that the internet discussions point to conflicting activities in cannabis where the beneficial effects for liver conditions lie
in the cannabidiol molecule as opposed to THC ligands which allegedly accelerate deterioration. I am just beginning research on this aspect. The
attached abstract has some of the information I'm asking about and I will ask for the ref in the appropriate forum.
Thanks for any and all pointers.
CRX
Attachment: CB-1 antagonism abstract.pdf (12kB)
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crazyboy - 28-1-2013 at 18:09
You seem to be confused about some terminology. Agonists are compounds that activate the neuronal receptor that it attaches to; antagonists attach to
a receptor but does not activate it or if it displaces an agonist at that receptor it seemingly deactivates it thereby reversing the effect of the
agonist. Cannabis contains cannabinoids which are CB1 and or CB2 agonists, the agonism of the CB1 and CB2 receptors results in the feelings associated
with being high.
Rimonabant is a CB1 inverse antagonist meaning it binds to the same receptor as an agonist but induces a pharmacological response opposite to that
agonist. For example CB1 and CB2 agonist cause increased appetite known sometimes as the munchies among other affects. Rimonabant causes appetite
suppression.
Just based on the information given I would guess cannabis or CB1 CB2 agonists would be detrimental to someone with hepatic fibrosis.
hissingnoise - 29-1-2013 at 06:39
I find it 'somewhat' ironic that a common herb, demonised since 1937, to a point where a sizable portion of the general public continues to view it with lingering, deep suspicion, though it's
beginning to have some of its unique properties uncovered, despite the fact that government-funded research in the US has been specifically aimed at
producing 'evidence' of cannabis's destructive toxicity is, at last, beginning to be seen in some medical circles, as a very potent medicine for hitherto intractable diseases . . .
chemrox - 29-1-2013 at 07:38
There seem to be conflicting forces at work. The endocannabinoid CB-1 antagonists such as cannabdiol seem to reverse fibrosis where as THC or
agonists seem to have a desultory effect. I believe cannabis indica is higher in CBD than sativa strains. I found the terminology confusing, yes.
I;m starting to get a little more clear about it.
chemrox - 29-1-2013 at 13:12
Here are a couple of articles that speak to CB-2 activation by THC and stellate apoptosis via cannabdiol. It's difficult to work out which data says
what when looking at the historic record. As earlier mentioned THC has been claimed as an accelerator of cirrohsis develpment. One wonders how much
Reagan/Bush era politics influenced those results. Also the problem of control in such studies. Small amounts of red wine has been proposed as a
valid treatment too. I suspect the population sampled has a large influence on the outcome when human subjects are reported. It would be good to
clear some of this up. Advocates of MM point to the articles that support a sort of "miracle drug" status for MM. One site I visited had a lot of
information on temperatures and forms of dispensation that appear to be well developed. If this subject is interesting to you take a look: http://www.rawhemp.tk/
[Edited on 29-1-2013 by chemrox]
Attachment: CB-2 activation by THC.pdf (15kB)
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zed - 11-6-2013 at 17:33
Some have suggested Ginkoloids may be helpful. Likewise Stem cells.