A study published in the peer reviewed journal Cannabis and Cannabinoid Research and available online through the U.S. National Library of Medicine explores the effects of Cannabistilbene I (a compound found in cannabis) on Angiotensin II (Ang II)-induced cardiac hypertrophy.
The research, conducted by a team at the University of Alberta, examined how Cannabistilbene I influences cytochrome P450 (CYP) enzymes and arachidonic acid (AA) metabolic pathways, both of which play crucial roles in heart function and hypertrophy. The study is titled Effect of Cannabistilbene I in Attenuating Angiotensin II-Induced Cardiac Hypertrophy: Insights into Cytochrome P450s and Arachidonic Acid Metabolites Modulation.
Cardiac hypertrophy is a condition in which the heart muscle enlarges due to stress, potentially leading to severe cardiovascular diseases. Therapeutic interventions targeting the underlying mechanisms, such as CYP enzymes and AA metabolites, could offer new ways to manage or prevent this condition.
To assess the impact of Cannabistilbene I, researchers used a cultured adult human ventricular cardiomyocyte cell line (AC16), which was treated with Cannabistilbene I in the presence and absence of Ang II. The team measured changes in mRNA expression related to cardiac hypertrophy markers and CYP enzymes through real-time polymerase chain reaction (PCR). Additionally, CYP protein levels were evaluated using Western blot analysis, while AA metabolites were quantified through liquid chromatography-tandem mass spectrometry (LC-MS/MS).
“Results showed that Ang II triggered hypertrophy, as evidenced by the increase in hypertrophic marker expression, and enlarged the cell surface area, effects that were alleviated by Cannabistilbene I”, states the study. “Gene expression analysis indicated that Cannabistilbene I upregulated CYP1A1, leading to increased enzymatic activity, as evidenced by 7-ethoxyresorufin-O-deethylase assay. Furthermore, LC-MS/MS analysis of AA metabolites revealed that Ang II elevated midchain (R/S)-hydroxyeicosatetraenoic acid (HETE) concentrations, which were reduced by Cannabistilbene I. ”
Notably, Cannabistilbene I “selectively increased 19(S)-HETE concentration and reversed the Ang II-induced decline in 19(S)-HETE, suggesting a unique protective role.
The study concludes by stating:
This study provides new insights into the potential of Cannabistilbene I in modulating AA metabolites and reducing Ang II-induced cardiac hypertrophy, revealing a new candidate as a therapeutic agent for cardiac hypertrophy.
