Time-Dependent Protection of CB2 Receptor Agonist in Stroke.

Posted on July 19, 2015 by David

“Recent studies have indicated that type 2 cannabinoid receptor (CB2R) agonists reduce neurodegeneration after brain injury through anti-inflammatory activity.

The purpose of this study was to examine the time-dependent interaction of CB2R and inflammation in stroke brain.

In conclusion, our data support a time-dependent neuroprotection of CB2 agonist in an animal model of stroke.

Delayed post- treatment with PPAR-γ agonist induced behavioral recovery and microglial suppression; early treatment with CB2R agonist suppressed neurodegeneration in stroke animals.”

http://www.ncbi.nlm.nih.gov/pubmed/26186541

http://www.thctotalhealthcare.com/category/stroke-2/

Interaction between Cannabinoid Compounds and Capsazepine in Protection against Acute Pentylenetetrazole-induced Seizure in Mice.

Posted on July 19, 2015 by David

“The pharmacological interaction between cannabinoidergic system and vanilloid type 1 (TRPV1) channels has been investigated in various conditions such as pain and anxiety.

In some brain structure including hippocampus, CB1 and TRPV1 receptors coexist and their activation produces opposite effect on excitability of neurons.

In this study, we tested the hypothesis that TRPV1 channel is involved in the modulation of cannabinoid effects on pentylenetetrazole (PTZ)-induced seizure threshold…

The anticonvulsant actions of both capsazepine and ACEA were attenuated after co-administration of these compounds. Moreover, the anticonvulsant action of capsazepine was attenuated after co-administration with VDM11.

The results suggest an interaction between cannabinoidergic system and TRPV1 receptors in protection against acute PTZ-induced seizure in mice.”

http://www.ncbi.nlm.nih.gov/pubmed/26185513

Endocannabinoid 2-arachidonylglycerol protects primary cultured neurons against homocysteine-induced impairments in rat caudate nucleus through CB1 receptor.

Posted on July 17, 2015 by David

“Homocysteine (Hcy) is a high risk factor for Alzheimer’s disease (AD). Caudate nucleus (CN), the major component of basal ganglia in the brain, is also involved in many neurological disorders.

2-Arachidonoylglycerol (2-AG), the true natural ligand for cannabinoid type-1 (CB1) receptors and the most abundant endogenous cannabinoid, has been shown to exhibit neuroprotective effects through its anti-inflammatory action from proinflammatory stimuli in the hippocampus and CN.

In the present work, we explored that 2-AG significantly protects CN neurons in culture against Hcy-induced response.

2-AG is capable of inhibiting elevation of Hcy-induced cyclooxygenase-2 expression associated with nuclear factor-kappaB/p38MAPK/ERK1/2 signaling pathway through CB1 receptors-dependent way in primary cultured CN neurons.

Our study reveals the therapeutic potential for 2-AG for the treatment of neurodegenerative diseases, such as AD.”

http://www.ncbi.nlm.nih.gov/pubmed/25007951

The Endocannabinoid System in Renal Cell: Regulation of Na+ Transport by CB1 Receptors Through Distinct Cell Signaling Pathways.

Posted on July 17, 2015 by David

“The function of the endocannabinoid system (ECS) in the renal tissue is not completely understood.

We studied the effect of compounds modulating the activity of cannabinoid CB receptors on the active reabsorption of Na+ in LLC-PK1 cells.

CONCLUSION AND IMPLICATIONS: ECS is expressed in LLC-PK1 cells. Both TRPV1 and CB1 regulate (Na++K+)-ATPase activity in these cells, and are modulated by lipid and peptide CB1 ligands, which act via different signaling pathways”

.http://www.ncbi.nlm.nih.gov/pubmed/25537261

The endocannabinoid system in renal cell: Regulation of Na+ transport by CB1 receptors through distinct cell signaling pathways.

Posted on July 17, 2015 by David

“The function of the endocannabinoid system (ECS) in the renal tissue is not completely understood. Kidney function is closely related to ion reabsorption in the proximal tubule, the nephron segment responsible for the reabsorption of 70- 80% of the filtrate.

We studied the effect of compounds modulating the activity of cannabinoid CB receptors on the active reabsorption of Na+ in LLC-PK1 cells.

CONCLUSION AND IMPLICATIONS:

ECS is expressed in LLC-PK1 cells. Both CB1 and TRPV1 regulate (Na+ +K+ )-ATPase activity in these cells, and are modulated by lipid and peptide CB1 ligands, which act via different signaling pathways.”

http://www.ncbi.nlm.nih.gov/pubmed/26177675

Sperm Release from the Oviductal Epithelium Depends on Ca2+ Influx Upon Activation of CB1 and TRPV1 by Anandamide.

Posted on July 2, 2015 by David

“The oviduct acts as a functional sperm reservoir in many mammalian species. Both binding and release of spermatozoa from the oviductal epithelium are mainly modulated by sperm capacitation. Several molecules from oviductal fluid are involved in the regulation of sperm function.

Anandamide is a lipid mediator involved in reproductive physiology. Previously, we demonstrated that anandamide, through activation of the cannabinoid receptor type 1 (CB1), promotes sperm release from bovine oviductal epithelial cells, and through CB1 and the transient receptor potential vanilloid 1 (TRPV1), induces sperm capacitation.

Our results also suggest that a phospholypase C (PLC) might mediate the activation of CB1 and TRPV1 in sperm release from the bovine oviduct.

Therefore, our findings indicate that anandamide, through CB1 and TRPV1 activation, is involved in sperm release from the oviductal reservoir. An increase of sperm Ca2+ levels and the PLC activation might be involved in anandamide signaling pathway. ”

http://www.ncbi.nlm.nih.gov/pubmed/26129689

Modulatory effects by CB1 receptors on rat spinal locomotor networks after sustained application of agonists or antagonists.

Posted on July 2, 2015 by David

“Sustained administration of cannabinoid agonists acting on neuronal CB1 receptors (CB1Rs) are proposed for treating spasticity and chronic pain…

Our data suggest that CB1Rs may control the circuit gateway regulating the inflow of sensory afferent inputs into the locomotor circuits, indicating a potential site of action for restricting peripheral signals disruptive for locomotor activity.”

http://www.ncbi.nlm.nih.gov/pubmed/26126926

Ultralow doses of cannabinoid drugs protect the mouse brain from inflammation-induced cognitive damage.

Posted on June 28, 2015 by David

“In our previous studies, we found that a single ultralow dose of tetrahydrocannabinol (THC)… protects the brain from different insults that cause cognitive deficits.

Because various insults may trigger a neuroinflammatory response that leads to secondary damage to the brain, the current study tested whether this extremely low dose of THC could protect the brain from inflammation-induced cognitive deficits…

Our results suggest that an ultralow dose of THC that lacks any psychotrophic activity protects the brain from neuroinflammation-induced cognitive damage and might be used as an effective drug for the treatment of neuroinflammatory conditions, including neurodegenerative diseases.”

http://www.ncbi.nlm.nih.gov/pubmed/25042014

An ultra-low dose of tetrahydrocannabinol provides cardioprotection.

Posted on June 24, 2015 by David

“Tetrahydrocannabinol (THC), the major psychoactive component of marijuana, is a cannabinoid agonist that exerts its effects by activating at least two specific receptors (CB1 and CB2) that belong to the seven transmembrane G-protein coupled receptor (GPCR) family.

Both CB1 and CB2 mRNA and proteins are present in the heart.

THC treatment was beneficial against hypoxia in neonatal cardiomyocytes in vitro.

We also observed a neuroprotective effect of an ultra low dose of THC when applied to mice before brain insults.

The present study was aimed to test and characterize the cardioprotective effects of a very low dose of THC…

All protocols of THC administration were found to be beneficial.

CONCLUSION:

A single ultra low dose of THC before ischemia is a safe and effective treatment that reduces myocardial ischemic damage.”

http://www.ncbi.nlm.nih.gov/pubmed/23537701

Delta-9-tetrahydrocannabinol protects cardiac cells from hypoxia via CB2 receptor activation and nitric oxide production.

Posted on June 24, 2015 by David

“Delta-9-tetrahydrocannabinol (THC), the major active component of marijuana, has a beneficial effect on the cardiovascular system during stress conditions…

The present study was designed to investigate the central (CB1) and the peripheral (CB2)cannabinoid receptor expression in neonatal cardiomyoctes and possible function in the cardioprotection of THC from hypoxia.

The antagonist for the CB2, but not CB1 receptor antagonist abolished the protective effect of THC.

In agreement with these results using RT-PCR, it was shown that neonatal cardiac cells express CB2, but not CB1 receptors.

Involvement of NO in the signal transduction pathway activated by THC through CB2 was examined. It was found that THC induces nitric oxide (NO) production by induction of NO synthase (iNOS) via CB2 receptors.

L-NAME (NOS inhibitor, 100 microM) prevented the cardioprotection provided by THC.

Taken together, our findings suggest that THC protects cardiac cells against hypoxia via CB2 receptor activation by induction of NO production.

An NO mechanism occurs also in the classical pre-conditioning process; therefore, THC probably pre-trains the cardiomyocytes to hypoxic conditions.”

http://www.ncbi.nlm.nih.gov/pubmed/16444588