|The human genome,
regardless of race, holds an informational blueprint capable of producing 17
different carbohydrate active enzymes (CAzymes1).
These CAzymes evolved
primarily to digest terrestrial plants, and took millions of years to develop.
The average human microbiome, on the other hand, is far more dynamic,
and contains many orders of magnitude more CAzymes than the generically shared
human genome is capable of producing itself.
One study estimated there
are about 16,000 different CAzymes in the human gut microbiome.
human gut symbiont Bacteroides thetaiotaomicron3, alone, contains 261
carbohydrate-digesting enzymes known as glycoside hydrolases and polysaccharide
|The human body hosts an
enormous abundance and diversity of microbes, which perform a range of
essential and beneficial functions.
Our appreciation of the importance
of these microbial communities to many aspects of human physiology has grown
dramatically in recent years.
Achieving a better understanding of the
contribution of the microbiome to mental health will require further
development of analytical approaches.
Developmental pathways must also
take into consideration points of interaction with our resident microbiota.
Refining these models based on empirical data now represents a key
challenge in understanding the processes behind altered brain function and
Anandamide and 2-AG have been
shown to inhibit the inflammatory processes triggered upon activation of the
toll-like receptor complex CD14/TLR4/MD2 (i.e., LPS and carrageenan
The same effect has also been reported for
other CB2 receptor agonists like JWH133,12 HU-308,13 and
human monocytic cell neurotoxicity and cytokine secretion by ligands of the
cannabinoid-type CB2 receptor
Alkylamides from Echinacea
are a new class of cannabinomimetics
Conclusion: The endogenous cannabinoid system is
physiologically involved in the protection against excessive inflammation in
the colon, both by dampening smooth muscular irritation caused by inflammation
and by controlling cellular pathways leading to inflammatory responses. These
results strongly suggest that modulation of the physiological activity of the
endogenous cannabinoid system during colonic inflammation might be a promising
therapeutic tool for the treatment of several diseases characterized by
inflammation of the gastrointestinal tract.
Conclusion: Pharmacological elevation of
endocannabinoid levels may be a promising strategy to counteract intestinal
inflammation and colon
The two forms of IBD,
colitis (UC) and Crohn's disease (CD) have rapidly increased in the past
years in Western countries ranging at a prevalence of more than 200 cases per
Initially, restitution is achieved by epithelial
dedifferentiation and migration, followed by proliferation, and, finally,
maturation. LPA has been shown to enhance intestinal epithelial wound
healing through increased epithelial cell migration.
Conclusion: Cannabinoids as a new gastric cancer
Conclusion: Cannabinoids as a good palliative agent
for cancer patients receiving paclitaxel.
Conclusion: Our study showed that CBD induces
apoptotic cell death in gastric cancer cells, which is triggered by ER stress
generation and subsequent XIAP inhibition by Smac (Fig. 7). Taken together, our
results suggest the potential of CBD in novel treatments against gastric
To study the effect of CBD on gastric cancer in
vitro, we treated the gastric cancer SGC-7901 cells with different
concentrations of CBD for 24 and 48 h. These results indicated that CBD could
effectively induce cell cycle arrest at the G0G1 phase by inhibiting CDK2
and cyclin E expression. We found that as the concentration of CBD increased,
the percentage of apoptotic cells in the SGC-7901 population increased (Figure
4b,c). These results indicated that CBD effectively induced apoptosis in
chronic liver disease
Conclusion: The EC system is strongly up-regulated
during chronic liver diseases. Until now it has been implicated in the
pathogenesis of fatty liver
disease associated with
alcohol abuse, and
in the progression of fibrosis to cirrhosis, and in the
development of portal
hypertension, hyperdynamic circulatory syndrome and its complications, and
cirrhotic cardiomyopathy. Furthermore, the EC system can participate in the
pathogenesis of acute liver injury by modulating the mechanisms responsible for
cell injury and inflammatory response. Thus, targeting the CB1 and
CB2 receptors represents a potential therapeutic goal for the
treatment of liver diseases.
Conclusion: Endocannabinoid-based therapies,
combining CB2 agonists and CB1 antagonists may open novel
therapeutic perspectives for the treatment of chronic liver diseases.
Conclusion: CB1 receptors have been
implicated in the pathogenesis of several lesions such as liver fibrogenesis,
alcoholic and metabolic steatosis, or circulatory failure associated with
cirrhosis. In contrast, stimulation of hepatic CB2 receptors is
emerging as an overall protective pathway with antifibrogenic properties and
beneficial effects on liver inflammation, alcoholic fatty liver and hepatocyte
survival and regeneration.
Conclusion: CB2 receptors reduce liver
injury and promote liver regeneration following acute insult, via distinct
paracrine mechanisms involving hepatic myofibroblasts.
Conclusion: Our study shows that CB1
receptor antagonists hold promise for the treatment of liver fibrosis.
Conclusion: CBD can alleviate lipid accumulation in
both an in vitro HepG2 cell model and an in vivo binge alcohol treatment model
by multiple mechanisms.
Conclusion: These findings demonstrate that
CB2 receptors display beneficial effects on alcohol-induced
inflammation by regulating M1/M2 balance in Kupffer cells, thereby reducing
hepatocyte steatosis via paracrine interactions between Kupffer cells and
Conclusion: Our results suggest that THCV and CBD
might be used as new therapeutic agents for the pharmacological treatment of
obesity- and metabolic
JWH-015-induced autophagy and apoptosis relies on CB2 receptor
Δ9-THC and JWH-015 inhibit the growth of the
human HCC lines HepG2 and HuH-7 via autophagy stimulation
and TRB3 upregulation involved Δ9-THC- and JWH-015-induced
autophagy and apoptosis of HCC cells
AMPK and TRB3 regulate
cannabinoid-induced autophagy of HCC cells through different
Activation of AMPK by cannabinoids relies on CAMKK
Conclusion: Cannabinoids have great promise as
treatments for nausea and that their anti-nausea effects may be mediated by the
interoceptive insular cortex.
Conclusion: This model may be a useful tool for
elucidating the neurobiology of nausea and the role that the endocannabinoid
system plays in the regulation of this distressing condition.
Conclusion: Future efforts aimed at developing new
endocannabinoid-based anti-nausea and anti-emetic therapies are clearly
Conclusion: Our data suggest
a possible implication of
the endocannabinoid system in the physiology and development of the human
Conclusion: CB1 has a major role in the
activation of myofibroblasts and may be a new target for treating
Cannabidiol, a safe and non-psychotropic ingredient
of marijuana, exerts pharmacological effects (e.g., antioxidant) and mechanisms
(e.g., inhibition of endocannabinoids enzymatic degradation) potentially
beneficial for the inflamed gut.
Conclusion: A short course (8 weeks) of THC-rich
cannabis produced significant clinical, steroid-free benefits to 10 of 11
patients with active Crohn's disease, compared with
placebo, without side effects.
As with the eCB system, many eCBome members regulate
several physiological processes, including energy intake and storage,
glucose and lipid
metabolism and pancreatic health,
which contribute to the development of type 2 diabetes (T2D). Preclinical
studies increasingly support the notion that targeting the eCBome may
beneficially affect T2D. The eCBome is implicated in T2D at several levels and
in a variety of tissues, making this complex lipid signaling system a potential
source of many potential therapeutics for the treatments for T2D.
Activation of CB-1 receptors in the gastrointestinal
tract may also be relevant
for the pathogenesis of obesity. The response of circulating ghrelin to
fasting was diminished with rimonabant, suggesting that CB-1 receptors are
involved in ghrelin secretion