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cbd ncbi

Further research manuscripts were retrieved through the reference lists of selected articles, and reports were found on international agencies or institutional websites including US FDA, WHO, US DEA, and US National Academies of Sciences, Engineering, and Medicine. All articles were screened independently by three co-authors to determine their relevance and included if selected by at least two co-authors.

Following 90 days of oral CBD (30-300 mg/kg/day), liver and kidney weights in rhesus monkeys were 13-56% greater than controls, without morphological changes in the organs [61].

1.7. Spasticity

In adults with chronic pain, patients treated with cannabis or cannabinoids are more likely to experience a clinically significant reduction in pain symptoms [24]. A recent review of specific cannabinoids and cannabinoid extracts on multiple pain types investigates both the preclinical and clinical data supporting cannabinoid pharmacotherapy for pain [46].

3.1.1. In Vitro Neurological Effects

There is tremendous interest in CBD as an anticancer agent. Aviello et al. showed that CBD had multiple chemopreventive effects in murine colorectal carcinoma cell lines by protecting DNA from oxidative damage, increasing endocannabinoid concentrations and reducing cell proliferation in a CB1-, TRPV1- and PPARγ-antagonists sensitive manner [47]. De Petrocellis et al. found that 1-10 µM CBD significantly inhibited human prostate carcinoma cell viability, inducing apoptosis and elevation of reactive oxygen species (ROS) [48]. Exciting new developments for enhancing CBD effects in inducing cell death and enhancing radiosensitivity of glioblastoma (GBM) cells were recently published [49]. GBM cells treated with CBD, γ-irradiation, and KU60019, an ATM kinase inhibitor, increased apoptosis and with strongly upregulated arrested cells, blockade of cell proliferation, and production of pro-inflammatory cytokines, improving CBD effectiveness.

Cbd ncbi

Given that CBD preparations containing substantial amounts of CBD are taken by a large number of individuals, we examined whether CBD exposure might correlate to a decreased risk of SARS-CoV-2 infection. Analysis of over 93,000 patients tested for SARS-CoV-2 at the University of Chicago Medical Center showed that 10.0% tested positive overall, but only 5.7% of the

Future studies to explore the optimal means of CBD delivery to patients along with clinical trials will be needed to fully test the promise of CBD as a therapeutic to block SARS-CoV-2 infection. As the clearance rates for CBD in plasma are substantially lower in humans than mice, we would suggest moving to clinical trials rather than doing preclinical studies in animal models ( 15 ). We advocate carefully designed placebo-controlled clinical trials with known concentrations and highly-characterized formulations in order to define CBD’s role in preventing and treating early SARS-CoV-2 infection. The necessary human in vivo concentration and optimal route and formulation remain to be defined. We strongly caution against the urge to take CBD in presently available formulations as a preventative or treatment therapy at this time, especially without the knowledge of a rigorous randomized clinical trial with this natural product ( 23 ).

Supplementary Material

National Institutes of Health grant R01 CA219815 (S.A.O.)

National Institutes of Health grant R01 AI137514 (G.R.)

ACKNOWLEDGEMENTS

A549-ACE2 cells were infected with SARS-CoV-2 at MOI of 3 with or without CBD treatment at 10 μM for 24 hours. RNA-seq was performed as described in Methods. (A) Heatmap of relative levels of SARS-CoV-2 genes from the RNA-seq samples. (B) Expression levels of SARS-CoV-2 spike and nucleocapsid genes. Percent expression level changes for genes from infected cells compared to cells infected and CBD treated are indicated for each gene. (C) Principal component analysis (PCA) of RNA-seq data showing control (veh_mock), SARS-CoV-2 infected (veh_infect), CBD-treated (CBD_mock), and SARS-CoV-2 infected plus CBD treated (CBD_infect) samples. The first and second principal components (PC1 and PC2) of each sample are plotted. (D) Heatmap of normalized expression levels of 5,000 most variable genes across all RNA-seq samples, clustered into 6 groups based on differential expression between treatment conditions.