Cannabis compound tackles blood vessel disease


The main compound in cannabis can prevent blood vessels from developing atherosclerosis, an inflammatory condition that is the primary cause of heart disease and stroke in the developed world.

(I-Newswire) April 13, 2005 - A study in this week's Nature shows that disease progression is halted when mice are given low doses of delta-9-tetrahydrocannabinol (THC).

Atherosclerosis occurs when the accumulation of immune cells in blood vessels causes narrowing of the arteries, lipid accumulation and plaque formation. THC prevents immune cell recruitment by binding to proteins called CB2 receptors on the cell surface, report François Mach and colleagues. When given chemicals that prevent THC binding to these receptors, the therapeutic effect of THC is abolished and the mice continue to develop disease symptoms.

In the brain, THC binds to a different cell-surface receptor, called CB1. The THC doses given to the mice (about 1 milligram per kilogram body weight per day) were lower than the level required to activate the CB1 receptor, so the psychoactive effects of cannabis were not observed. This suggests that a possible treatment for atherosclerosis might be to use pure, isolated THC - this would avoid other harmful effects of cannabis, such as increased blood pressure. "These findings should not be taken to mean that smoking marijuana is beneficial for the heart," writes Michael D. Roth in a related News and Views article.

http://nature.com/nature (pp 782-786; N&V)

ALSO IN THIS ISSUE…

[11] Modes of faulting at mid-ocean ridges (pp 719-723)

[12] Generation and annotation of the DNA sequences of human chromosomes 2 and4 (pp 724-731)

[13] Recruitment of entomopathogenic nematodes by insect-damaged maize roots (pp 732-737)

[14] Water content in the transition zone from electrical conductivity of wadsleyite and ringwoodite (pp 746-749)

[15] Particle size and energetics of gouge from earthquake rupture zones (pp 749-752)

[16] Impairment of angiogenesis and cell migration by targeted aquaporin-1 gene disruption (pp786-792)

ADVANCE ONLINE PUBLICATION

***This paper will be published electronically on Nature's website on 6 April at 1800 London time / 1300 US Eastern time (which is also when the embargo lifts) as part of our AOP (ahead of print) programme. Although we have included it on this release to avoid multiple mailings it will not appear in print on 7 April, but at a later date.***

[17] Spatiotemporal regulation of MyD88-IRF-7 signalling for robust type-I interferon induction
DOI: 10.1038/nature03547

Reference URL
http://nature.com/nature

SOURCE: http://www.alphagalileo.org



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