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cbd hemp oil for copd

In most cases, treatment for COPD patients is multifaceted. Lifestyle changes [6] may be required on top of medication, rehabilitation, and therapy. In severe cases, some COPD patients require surgery or lung transplant. Unfortunately, if your COPD is caused by smoking, you may not be eligible for a lung transplant until you’ve stopped smoking for at least 6 months. Smoking, drinking, and using drugs can increase the risk of health problems for a transplant patient.

The goal of therapy for people with COPD is to stop the progression of the disease and to improve lung function. A combination of oxygen therapy and pulmonary rehabilitation can go a long way in improving the symptoms of various lung diseases like COPD, but other symptoms can be a little more stubborn.

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Does CBD Help COPD?

When shopping for CBD products, it is important to do your research to know exactly what you’re purchasing. Many CBD products contain traces of THC [9] . In fact, it is legal in most states for CBD products to contain up to 0.3% THC by dry weight. You should also ensure the CBD products you choose are made with high-quality CBD and that the products have been tested by a third-party lab for purity and safety.

Another study conducted on guinea pigs in 2014 [16] supports this hypothesis, showing reduced inflammation, cough, and improved lung function in the guinea pigs with damaged lungs treated with THC.

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After the yield of RNA extraction was quantified using a Nanodrop (Thermo Fisher Scientific), complementary DNA (cDNA) was synthesized from 250 ng of RNA using the reverse transcription (RT2) First Strand kit (Qiagen, Valencia, CA) following the manufacturer’s instructions.

The extract induced significant (P < 0.05) changes in expression of 37 tested genes. Six genes (CSF2, IL1RL1, IL4, IL13RA2, IL17A and PPARG) were up-regulated at all three dilutions. Another two (CCL22 and TSLP) were up-regulated while six (CLCA1, CMA1, EPX, LTB4R, MAF and PMCH) were down-regulated at the 1:400 and 1:800 dilutions. The relationship of differentially-expressed genes of interest to biologic pathways was explored using the Database for Annotation, Visualization and Integrated Discovery (DAVID).

Cell culture

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.

Quantitative PCR results were analyzed by the delta cycle threshold (Ct) method, with the 0.25% ethanol treated cells as a control, using the Data Resources Center (www.Qiagen.com). Genes with Ct values > = 35 were excluded from this analysis, and genes with Ct values > 32 were considered low expression. Fold changes (2^(− Delta Ct)) were determined as the normalized gene expression (2^(− Delta Ct)) in the cannabis extract treated sample divided by the normalized gene expression (2^(− Delta Ct)) in the control sample (ethanol treated cells). Student’s t-test was used to determine p-values between control group (ethanol) and each experimental group (cannabis oil extract). Genes were regarded as up-regulated or down-regulated if their extract treatment fold changes were > 2.0 or < 0.5 relative to ethanol controls and were statistically significant (P < 0.05). The same analysis was performed to compare the results of the 0.25% ethanol treated cells with that of the saline control cells.

Treatment of HSAEpC cells with cannabis oil extract markedly altered expression of 37 immune response and related genes out of 84 tested after 24 h of treatment. Some of these genes are known in the literature to be associated with respiratory diseases such as COPD. Bioinformatics analysis using the DAVID program was helpful in elucidating groups of genes with related biological activities. For example, 11 GOIs were part of the same KEGG pathway for cytokine and cytokine receptor interactions. This pathway is important in the early recognition and response phases of both innate and adaptive immunity (Arakelyan et al. 2017; Gardy et al. 2009). Furthermore, out of 26 respiratory disease-related GOIs, there were 10 GOIs specifically related to COPD. This bioinformatics analysis was coupled with literature evaluations in order to highlight the most relevant of these genes. The logical starting point for this was the eight GOIs that were up-regulated at two or three test dilutions (Tables 1 and 4), along with the six GOIs that were down-regulated at two test dilutions (Table 2).