Comparison of Cannabidiol, Antioxidants, and Diuretics in Reversing Binge Ethanol-Induced Neurotoxicity

“Alcohol is the world’s most widely used psychoactive drug, but chronic, excessive alcohol consumption leads to permanent organ damage or death..

In the current study, we use a rat model of binge alcohol consumption to determine the potential of cannabidiol (CBD) as a neuroprotectant against ethanol-induced neurotoxicity…

…we evaluated CBD as a neuroprotectant in a rat binge ethanol model.

When administered concurrently with binge ethanol exposure, CBD protected against hippocampal and entorhinal cortical neurodegeneration in a dose-dependent manner.

This study provides the first demonstration of CBD as an in vivo neuroprotectant…

CBD protects against binge alcohol-induced damage.”

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Targeting the endocannabinoid system to treat haunting traumatic memories

“One of the core symptoms in post-traumatic stress disorder (PTSD) is the traumatic memory that constantly haunts the patient.

An increasing body of evidence points to the endocannabinoid (eCB) system as a key system in the regulation of emotionality and memory.

Hence, eCB enhancers may be the ideal pharmacological treatment for PTSD…

…eCBs have an essential role in maintaining emotional homeostasis and in modulating memory consolidation, retrieval and extinction.

Hence, the authors concluded that eCBs could be an ideal drug to treat PTSD by addressing both the emotional and cognitive aspects of the disorder.

Indeed, accumulating data from both clinical and pre-clinical studies suggest that targeting the eCB system may benefit PTSD.

Several studies support the self-medication hypothesis explanation for cannabis use to cope with PTSD symptoms.

To conclude, the eCB system may be a useful target for treating both the cognitive and emotional features of PTSD…”

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Cannabinoids inhibit migration of microglial-like cells to the HIV protein Tat.

“Microglia are a population of macrophage-like cells in the central nervous system (CNS) which, upon infection by the human immunodeficiency virus (HIV), secrete a plethora of inflammatory factors, including the virus-specified trans-activating protein Tat.

Tat has been implicated in HIV neuropathogenesis since it elicits chemokines, cytokines, and a chemotactic response from microglia. It also harbors a β-chemokine receptor binding motif, articulating a mode by which it acts as a migration stimulus.

Since select cannabinoids have anti-inflammatory properties, cross the blood-brain barrier, and target specific receptors, they have potential to serve as agents for dampening untoward neuroimmune responses.

The aim of this study was to investigate the effect of select cannabinoids on the migration of microglial-like cells toward Tat.

…it was demonstrated that the exogenous cannabinoids Delta-9-tetrahydrocannabinol (THC) and CP55940 exerted a concentration-related reduction in the migration of BV-2 cells towards Tat.

These results indicate that cannabinoid-mediated inhibition of BV-2 microglial-like cell migration to Tat is linked functionally to the CB2R…”

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Cannabinoid inhibition of macrophage migration to the trans-activating (Tat) protein of HIV-1 is linked to the CB(2) cannabinoid receptor.

“Macrophages and macrophage-like cells are important targets of HIV-1 infection at peripheral sites and in the central nervous system…


Collectively, the pharmacological and biochemical knockdown data indicate that cannabinoid-mediated modulation of macrophage migration to the HIV-1 Tat protein is linked to the CB(2)cannabinoid receptor.

Furthermore, these results suggest that the CB(2) cannabinoid receptor has potential to serve as a therapeutic target for ablation of HIV-1-associated untoward inflammatory response.”


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Chronic administration of Δ9-tetrahydrocannabinol induces intestinal anti-inflammatory microRNA expression during acute SIV infection of rhesus macaques.

“In SIV-infected macaques, chronic administration of Δ9-tetrahydrocannabinol (Δ9-THC), inhibited viral replication, intestinal inflammation and slowed disease progression.

Persistent gastrointestinal disease/inflammation has been proposed to facilitate microbial translocation, systemic immune activation and promote disease progression. Cannabinoids including Δ9-THC attenuated intestinal inflammation in mouse colitis models and SIV-infected rhesus macaques…

Gastrointestinal tract (GI) disease/inflammation is a hallmark of HIV/SIV infection. Previously, we showed that chronic treatment of SIV-infected macaques with Δ9 tetrahydrocannabinol (Δ9-THC) increased survival and decreased viral replication and infection induced gastrointestinal inflammation.

Here, we show that chronic THC administration to SIV-infected macaques induced an anti-inflammatory microRNA expression profile…

Overall, our results show that selective upregulation of anti-inflammatory miRNA expression, contributes to THC-mediated suppression of gastrointestinal inflammation and maintenance of intestinal homeostasis.”

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Cannabidiol improves lung function and inflammation in mice submitted to LPS-induced acute lung injury.

“We have previously shown that the prophylactic treatment with cannabidiol (CBD) reduces inflammation in a model of acute lung injury (ALI).

In this work we analyzed the effects of the therapeutic treatment with CBD in mice subjected to the model of lipopolysaccharide (LPS)-induced ALI on pulmonary mechanics and inflammation…

The results show that CBD decreased total lung resistance and elastance, leukocyte migration into the lungs, myeloperoxidase activity in the lung tissue, protein concentration and production of pro-inflammatory cytokines (TNF and IL-6) and chemokines (MCP-1 and MIP-2) in the bronchoalveolar lavage supernatant.

Thus, we conclude that CBD administered therapeutically, i.e. during an ongoing inflammatory process, has a potent anti-inflammatory effect and also improves the lung function in mice submitted to LPS-induced ALI.

Therefore the present and previous data suggest that in the future cannabidiol might become a useful therapeutic tool for the attenuation and treatment of inflammatory lung diseases.”

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Cannabinoid Type 1 and Type 2 Receptor Antagonists Prevent Attenuation of Serotonin-Induced Reflex Apneas by Dronabinol in Sprague-Dawley Rats.

“The prevalence of obstructive sleep apnea (OSA) in Americans is 9% and increasing…

Vagal afferent neurons are inhibited by cannabinoid type 1 (CB1) or cannabinoid type 2 (CB2) receptors in animal models of vagally-mediated behaviors…

These findings underscore the therapeutic potential of dronabinol (THC) in the treatment of OSA and implicate participation of both cannabinoid receptors in dronabinol’s apnea suppression effect.”

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[There is evidence for the use of cannabinoids for symptomatic treatment of multiple sclerosis.]

“We identified 16 randomized placebo-controlled trials investigating cannabinoids as symptomatic treatment in multiple sclerosis (MS).

There is evidence that nabiximols (THC/CBD) oromucosal spray may reduce subjective symptoms of spasticity and that dronabinol (THC) is effective against neuropathic pain in patients with MS…”

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The interface: marijuana and body weight.

“Acute marijuana use is classically associated with snacking behavior (colloquially referred to as “the munchies”). In support of these acute appetite-enhancing effects, several authorities report that marijuana may increase body mass index in patients suffering from human immunodeficiency virus and cancer…

Marijuana is a clinically controversial substance, but one potential medical benefit may be weight gain. According to available studies, appetite stimulation as well as weight gain may occur in patients with physical debilitation due to HIV/AIDS and/or cancer.

As for the effects of marijuana on body weight in the general population, use appears to be associated with a lower body mass index.

…marijuana may genuinely be a regulatory compound, increasing weight in those with low weight, but not in those who are normal or overweight.”

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Cannabidiol: promise and pitfalls.

“Over the past few years, increasing public and political pressure has supported legalization of medical marijuana.

One of the main thrusts in this effort has related to the treatment of refractory epilepsy-especially in children with Dravet syndrome-using cannabidiol (CBD).

Despite initiatives in numerous states to at least legalize possession of CBD oil for treating epilepsy, little published evidence is available to prove or disprove the efficacy and safety of CBD in patients with epilepsy. This review highlights some of the basic science theory behind the use of CBD, summarizes published data on clinical use of CBD for epilepsy, and highlights issues related to the use of currently available CBD products.

Cannabidiol is the major nonpsychoactive component of Cannabis sativa.

Over the centuries, a number of medicinal preparations derived from C. sativa have been employed for a variety of disorders, including gout, rheumatism, malaria, pain, and fever.

These preparations were widely employed as analgesics by Western medical practitioners in the 19(th) century.

More recently, there is clinical evidence suggesting efficacy in HIV-associated neuropathic pain, as well as spasms associated with multiple sclerosis.”

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