Research conducted by the University of Alberta and Canurta collaborators dives into how cannflavin-C, a natural compound derived from the cannabis sativa plant, affects angiotensin II (Ang II)-induced cardiac hypertrophy. This condition involves the enlargement of heart cells, which is a characteristic feature of heart diseases.
Using human ventricular cardiomyocytes (AC16 cells), the research team observed that cannflavin-C counteracts the effects of Ang II. It reduces the expression of hypertrophic markers such as myosin heavy chain (β/α-MHC), atrial natriuretic peptide (ANP), and brain natriuretic peptide (BNP), and inhibits the enlargement of cell surface area.
The study also uncovered that cannflavin-C acts by downregulating cytochrome P450 1B1 (CYP1B1), an enzyme critical for metabolizing arachidonic acid (AA) into midchain hydroxyeicosatetraenoic acids (HETEs). This enzyme pathway is implicated in the progression of cardiac hypertrophy. Analysis using LC-MS/MS confirmed that cannflavin-C attenuates the rise in midchain (R/S)-HETEs concentrations induced by Ang II.
These findings highlight cannflavin-C as a promising therapeutic candidate for combating cardiac hypertrophy by modulating CYP1B1 and AA metabolites. This research opens new avenues for developing treatments aimed at conditions like heart failure.
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