جستجوی مقالات مرتبط با کلیدواژه « cannabinoids » در نشریات گروه « پزشکی »

Polycystic ovary syndrome (PCOS) is a complex metabolic and endocrine disorder associated with chronic inflammation. However, the effect of ∆9 Tetrahydrocannabinol (THC) on PCOS has not been evaluated.  Therefore, this study aimed to investigate the immunomodulatory effects of THC in an animal model of PCOS. 

Twenty female Sprague-Dawley rats, aged 4 weeks, were divided into four groups. The control group received a normal diet, the sham group received a vehicle (carboxymethyl cellulose), the PCOS group received a high-fat diet (HFD) for 16 weeks followed by letrozole for 4 weeks, and the THC group received an HFD for 16 weeks followed by letrozole+THC (0.02 mg/kg) for 4 weeks. 

The PCOS animals exhibited significantly higher levels of testosterone, insulin, triglycerides, and total cholesterol, along with elevated inflammatory and oxidative stress markers compared to the control group. Flow cytometry and real-time PCR analysis revealed an increase in M1 macrophage markers and a decrease in M2 macrophage markers compared to the control group. However, the administration of a low dose of THC mitigated these disturbances.

Low-dose THC improved inflammatory responses and shifted the balance of M1/M2 macrophage markers towards M2 macrophages in the animal model of PCOS.

The use of cannabis-derived compounds for medical purposes dates from more than two thousand years. Due to its psychotropic effects and cultural aspects related to the plant of origin, its benefits have been disregarded in several western countries. Nevertheless, the number of studies on Cannabis sativa, especially on clinical applications of cannabinoids, increased significantly in the latest years. Amidst the benefits of cannabis-derived compounds is pain relief. Here we review physiological, pharmacological and chemical aspects of pain management in humans with endocannabinoids, synthetic cannabinoids and phytocannabinoids. The analgesia mechanism can be explained not only through interactions with cannabinoid receptors 1 and 2 but also through direct or indirect interaction with serotonin, glycine, gamma-aminobutyric acid, N-methyl-D-aspartate, adrenergic and opioid receptors, as well as transient receptors potential channels. They can also modify the behavior of molecules such as cytokines, calcitonin gene-related protein and substance P, which largely influence pain-related mechanisms. Exogenous cannabinoids are interesting options to consider when it comes to pain management, especially in complex cases associated to poor response to the currently available drug therapy

Lung cancer remains a major factor contributing to morbidity and mortality worldwide. Apart from the chemotherapeutic agents in routine use, factors targeting novel molecular pathways are in clinical trials and provide hope for terminal lung cancer patients. The endocannabinoid system has recently become a popular field of study. Many experimental studies have shown that CBD and THC could be useful as a specific treatment for lung cancer since they play a major role in lung cancer cell apoptosis. The objective of this review was to evaluate the antitumorigenic mechanisms of CBD in lung cancer cells.

We searched the databases MEDLINE, clinicaltrials.gov, Cochrane Central Register of Controlled Trials, and Google Scholar using specific terms. A total of 246 studies were screened, and nine studies were included in the review. All the selected studies were conducted in vitro, and four of which also had an in vivo component. Included studies were assessed in our review using the ToxRTool.

The most common cell line used in all of the studies was A549; however, some studies contained other cell lines, including H460 and H358. We concluded that CBD has direct antineoplastic effects on lung cancer cells through various mechanisms mediated by cannabinoid receptors or independent of these receptors. All studies were referred to an in vitro model; hence, further research in animals is required, and if results remain promising, human clinical trials are ncessary.

CA1, as a major structure involved in learning and memory, has been shown to be affected by tramadol addiction. Both orexin and endocannabinoid receptors express in CA1 and play an important role in drug dependency. The aim of this study was to evaluate the modulatory effects of orexin‑2 (OX2R) and endocannabinoid‑1 (CB1R) receptors on neuronal activity in CA1, in response to tramadol in rats.

Male Wistar rats were divided into 8 groups (n = 6–7); saline‑dimethyl sulfoxide (DMSO), tramadol‑DMSO, saline‑TCS‑OX2‑29, saline‑AM251, tramadol‑TCS‑OX2‑29, tramadol‑AM251, saline‑TCS‑OX2‑29‑AM251, tramadol‑TCS‑OX2‑29‑AM251. Tramadol was injected intraperitoneally, and then, AM251 (1 nmol/0.3 μL), CB1R antagonist and TCS‑OX2‑29 (1 nmol/0.3 μL), OX2R antagonist, were microinjected individually or concurrently into the CA1. Using in vivo extracellular single‑unit recording, the firing of CA1 pyramidal neurons was investigated.

Tramadol decreased neuronal activity in CA1 (P < 0.01) but increased it after micro‑injection of DMSO. TCS‑OX2‑29 increased neuronal activity in saline group (P < 0.05) but decreased it in tramadol group. AM251 had no effect on saline group but decreased neuronal activity in tramadol group (P < 0.05). Concurrent micro‑injection of TCS‑OX2‑29 and AM251 had no effect on saline group but decreased neuronal activity in tramadol group (P < 0.05).

Our findings suggest that neural activity in CA1 is rapidly affected by acute use of tramadol, and some of these effects may be induced through the endocannabinoid and orexin systems. Thus, the function of endocannabinoid and orexin systems in CA1 may play a role in tramadol addiction.

Synthetic cannabinoids (SCs) are highly abused of New Psychoactive Substances (NPS). SCs has known under street names such as “Spice”, “herbal incense” and “K2”, act as endocannabinoids (CB) receptor full agonists and have unpredictable toxicity and abuse potential. This narrative review was conducted to update the present evidence about the clinical and forensic toxicological aspects of SCs.

PubMed, Scopus and Google Scholar  databases from 2015 to 2020 (up to 1st May) were searched using the terms “synthetic cannabinoids”, “synthetic cannabimimetics”, “ K2”,  “Spice”, “clinical toxicology”, “forensic toxicology”, “poisoning”, “toxicity”, “abuse” , “addiction “analysis” and “determination” to identify the relevant articles. In addition, a manual search of reference lists of the retrieved articles was conducted.

ADB-FUBINACA , XRL-11, 5F-ADB, 5F-PB-22, MDMB-CHMICA and MMB-2201 are the commonly reported SCs analogues among acute toxicities and fatalities cases. Adverse reactions and toxic effects of SCs includes psychoneurological, cardiovascular, renal and gastrointestinal involvements. Deaths related to SCs have been reported due to stroke and cardiac dysrhythmia. Analysis of SCs in biological samples in the clinical and postmortem setting needs sophisticated analytical instruments. Liquid gas chromatography tandem mass spectrometry (LC-MS/MS) has a crucial role for detection of SCs and their metabolites in biological samples.

Unlike natural cannabinoids, the SCs abuse/poisoning has serious and life-threatening effects in abuser. Also, analysis of SCs is not included in the routine forensic urine drug testing. Therefore, suitable measures of informing the public and health care professionals for prevention of SCs abuse are recommended.

Synthetic cannabinoid use such as “K2” and “Spice” is popular secondary to its inability to be detected in a urine drug screen. It is associated with a wide range of myocardial pathologies including obstructive and non-obstructive coronary disease such as Takotsubo cardiomyopathy.

A case report of an emancipated 15-year-old male experiencing Takotsubo cardiomyopathy after using the synthetic cannabinoid “Spice” is presented here.

Synthetic cannabinoids act as full agonists and bind to cannabinoid receptors (CB receptors) with a much greater potency compared to natural forms of marijuana. In particular, “Spice” decreases the release of glutamate via the CB receptor type 1 (CB1 receptor) in higher concentrations, which causes mitogen-activated protein kinase (MAPK) activation, substances released in response to stressful environments being experienced in the body. These effects can cause the sympathetic system to become activated by synthetic cannabinoid use, leading to a surge in catecholamines and a change from normal positive inotropy to abnormally-mediated negative inotropy. Use of synthetic cannabinoids can therefore be associated with Takotsubo cardiomyopathy. This case has important implications for additional examination secondary to the sparse information describing co-occurrence of Takotsubo cardiomyopathy and synthetic cannabinoid use.