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cbd oil and emphysema

My Thoughts on Royal CBD:

Given this, there are no specific dosage guidelines when it comes to using CBD oil for COPD.

Pros:

Best CBD Oils for COPD

Pros:

CBD has been studied for its anti-inflammatory effects and its efficacy as a bronchodilator. Both of these effects indicate that CBD may alleviate some of the symptoms of COPD.

Scientists in the 2014 study stated that “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,” suggesting that CBD could be an effective treatment for COPD.

COPD is an acronym for chronic obstructive pulmonary disease. This is a progressive lung disease that makes breathing increasingly difficult for patients over time.

Two up-regulated genes, CSF2 and IL17A, were identified in pathway analysis as positive regulators of IL-23 production. IL-23 is a pro-inflammatory cytokine involved in the cell-mediated immune response (Oppmann et al. 2000). This cytokine has been described as heterodimeric, composed of two subunits, IL-23A and IL-12B. Neither IL23 itself or IL23A were part of the gene array, but the IL12B gene, encoding interleukin 12B (natural killer cell stimulatory factor 2, cytotoxic lymphocyte maturation factor 2, p40) was up-regulated at the 1:400 dilution. IL17A (alternatively, IL17) encodes cytokine IL-17A, which, like IL-23, plays a role in inflammation (Chen and Kolls 2017). Increased production of IL-17A can occur in both asthma and COPD, and may contribute to COPD pathophysiology (Alcorn et al. 2010; Chang et al. 2014). However, IL-17A also functions in host defense against microbial pathogens (Aujla et al. 2007; Tsai et al. 2013). Perhaps a more interesting finding was that certain T-cell populations in asthma patients can produce both IL-17A and IL-4, and such cells appear to be a combination of Th17 (an immune response involving IL-17 and separate from Th1 and Th2) and Th2 (Cosmi et al. 2010).

Tables 1 and 2 show qPCR fold regulation data for individual genes whose expression was significantly (P < 0.05) up-regulated or down-regulated, respectively, by any of the three cannabis oil extract dilutions (1:400, 1:800 and 1:1600) at 24 h. Overall, of the 84 analyzed genes, 37 (16 up-regulated and 21 down-regulated) were affected by one or more cannabis oil extract dilutions. Treatment with the 1:400 dilution resulted in 15 up-regulated and 20 down-regulated genes, while the 1:800 dilution treatment yielded nine up-regulated and seven down-regulated genes. Six genes (CSF2, IL1RL1, IL4, IL13RA2, IL17A and PPARG) were up-regulated by all three extract dilutions, with fold changes ranging from three to over 180 (Table 1 and Fig. 1). There also were two genes (CCL22 and TSLP) that were up-regulated and six genes (CLCA1, CMA1, EPX, LTB4R, MAF and PMCH) that were down-regulated at both the 1:400 and 1:800 dilutions. Fold changes for the six down-regulated genes ranged between 0.45 and < 0.04 (Table 2 and Fig. 2). Of the 47 genes that were neither up- or down-regulated, 36 showed undetectable expression in both treatment and control samples, based on Ct values > 35. No data were obtained for one of the 84 genes, IL18, because of a technical error. The 1:800 dilution of cannabis oil extract was tested two additional times under slightly modified conditions, each with its own negative control. This was done to confirm and extend the initial observations. Results were similar to that of 1:800 dilution from the primary experiment (data not shown). Finally, the ethanol control was compared to the PBS control to determine if 0.25% ethanol had an effect on gene expression. The average fold change of the 84 genes tested was 0.89, and none were significantly up-regulated. Only one gene (IL17A) was significantly down-regulated (fold change = 0.4). Interestingly, IL17A was significantly up-regulated at all three extract dilutions.

After 24 h of exposure to cannabis oil extract, cells were washed with PBS, collected in Trizol (Thermo Fisher Scientific, Waltham, MA) and total mRNA was extracted following manufacturer’s instructions. Briefly, samples were incubated for 5 min at room temperature and 200 ul of chloroform (Sigma-Aldrich, Saint Louis, MO) was added to 1 ml of Trizol. The aqueous phase containing RNAs was separated by centrifugation at 12,000 g for 15 min and transferred in a new tube. RNA was subsequently precipitated by adding 500 ul of isopropanol (Sigma-Aldrich) for 10 min followed by centrifugation for 10 min at 12,000 g. Pellets containing RNAs were washed three times in 75% ethanol and resuspended in 15–40 ul of nuclease-free water.

DAVID bioinformatics analysis summary

Genes of interest (GOIs) up-regulated by cannabis oil extract at all three test dilutions (dose response experiment). HSAEpC were exposed to each of three dilutions of cannabis oil extract in ethanol for 24 h. Each fold change result is based on four cannabis oil extract treatment replicates and six control replicates. Legend: Black, 1:400 dilution; Grey, 1:800 dilution; Horizontal Stripes, 1:1600 dilution

HSAEpC were seeded in 6-well cell culture plates at a density of 200,000 cells per well. After overnight adhesion, cells were treated for 24 h with media containing cannabis oil extract (1:400, 1:800 and 1:1600 dilutions). Negative control cells were treated with an equivalent volume of ethanol or phosphate buffered saline (PBS) (1:400 dilution for a 0.25% final concentration). Each treatment dilution had four replicates, whereas control conditions (ethanol and PBS) had 6 replicates.

GOIs down-regulated by cannabis oil extract at the 1:400 and 1:800 test dilutions (dose response experiment). HSAEpC were exposed to each of three dilutions of cannabis oil extract in ethanol for 24 h. Each fold change result is based on four cannabis oil extract treatment replicates and six control replicates. There were no down-regulated genes at the 1:1600 dilution. Legend: Black, 1:400 dilution; Grey, 1:800 dilution

Two other GOIs down-regulated by cannabis oil extract that may have relevance to COPD were LTB4R (alternatively, BLT1 or LTB4R1), which encodes leukotriene B4 receptor, and EPX, which encodes eosinophil peroxidase. Leukotriene B4 is an arachidonic acid-derived, neutrophil recruiting, pro-inflammatory lipid molecule, and both this leukotriene and its receptor have a role in the pathophysiology of COPD (Dong et al. 2016; Marian et al. 2006; Pace et al. 2013). The targeting of the B4 receptor has been considered as a viable approach to the treatment of COPD (Grönke et al. 2008; Hicks et al. 2010). Accordingly, the down-regulation of LTB4R by cannabis oil extract appears to be yet another indication of its anti-inflammatory potential. Interestingly, PPAR-gamma, which was up-regulated by cannabis oil extract, can also counteract inflammation mediated by leukotriene B4 in COPD (Yin et al. 2014). While eosinophil peroxidase does not appear to have been investigated as target for the treatment of COPD, it has been identified as a biomarker of the disease (Nair et al. 2013; Yang et al. 2017).