Anti-inflammatory Effect of a Combination of Cannabidiol and Morinda citrifolia Extract on Lipopolysaccharide-stimulated RAW264 Macrophages
The inflammatory response plays an important role in the activation and progression of many inflammation-related diseases. Cannabis sativa and Morinda citrifolia have long been used in folk medicine to treat inflammation. Cannabidiol is the most abundant non-psychoactive phytocannabinoid in C. sativ...
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Published in | In vivo (Athens) Vol. 37; no. 2; pp. 591 - 595 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Greece
International Institute of Anticancer Research
01.03.2023
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Subjects | |
Online Access | Get full text |
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Summary: | The inflammatory response plays an important role in the activation and progression of many inflammation-related diseases. Cannabis sativa and Morinda citrifolia have long been used in folk medicine to treat inflammation. Cannabidiol is the most abundant non-psychoactive phytocannabinoid in C. sativa and exhibits anti-inflammatory activity. The objective of this study was to examine the anti-inflammatory effect of cannabidiol in combination with M. citrifolia and compare its effects with those of cannabidiol alone.
RAW264 cells stimulated with lipopolysaccharide (200 ng/ml) were treated with cannabidiol (0-10 μM), M. citrifolia seed extract (0-100 μg/ml), or a combination of both for 8 or 24 h. Following the treatments, nitric oxide production in the activated RAW264 cells and the expression of inducible nitric oxide synthase were assessed.
Our results showed that combination of cannabidiol (2.5 μM) and M. citrifolia seed extract (100 μg/ml) exhibited more efficient inhibition of nitric oxide production than cannabidiol treatment alone in lipopolysaccharide-stimulated RAW264 cells. The combination treatment also reduced the expression of inducible nitric oxide synthase.
These results suggest that the anti-inflammatory effect of combined treatment with cannabidiol and M. citrifolia seed extract causes a reduction in the expression of inflammatory mediators. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 |
ISSN: | 0258-851X 1791-7549 1791-7549 |
DOI: | 10.21873/invivo.13117 |