The role of exercise training and the endocannabinoid system in atherosclerotic plaque burden and composition in Apo-E-deficient mice

Abstract

Both exercise and rimonabant treatments induced plaque regression and promoted plaque stability. The combined treatment failed to show additive or synergistic benefits relative to either intervention alone.

Aerobic exercise attenuates dysautonomia, cardiac diastolic dysfunctions, and hemodynamic overload in female mice with atherosclerosis

“…The MAT performed aerobic exercise training on a treadmill at moderate intensity (60–75% of the maximum treadmill test). The ET was performed during the last 6 weeks of the protocol (5 days/week, 1 h/day) 20 .…”

Research progress in the management of vascular disease with cannabidiol: a review

“…However, CB1 promotes atherosclerosis, and its activation can promote the production of active oxygen metabolites and accelerate cell damage and death. Studies conducted by Katsimpoulas M et al showed that CB1 antagonists can promote the regression and stability of atherosclerotic plaque and reduce the incidence of cardiogenic stroke [ 48 ]. Since CB1, FAAH, and CB2 are all important components of ECS and have a close association with the therapeutic effect of CBD, we speculate that CBD plays a key role in regulating lipid metabolism.…”

“… [ 47 ] Mouse; ApoE-/- mice (n = 48); Exercise and rimonabant treatments Both exercise and rimonabant treatments induced plaque regression and promoted plaque stability. [ 48 ] Mouse; type I diabetic cardiomyopathy mouse model; CBD CBD could have a high therapeutic potential in the management of cardiovascular disorders by attenuating oxidative/nitrative stress, inflammation, cell death, and fibrosis. [ 53 ] Cell; Mouse microglial cells; CBD CBD exerted its anti-inflammatory effects on microglia via its intrinsic antioxidant properties, which are amplified by the inhibition of glucose-dependent NADPH synthesis.…”

The Endocannabinoid System and Cannabidiol: Past, Present, and Prospective for Cardiovascular Diseases

“…The classical eCBs, i.e., AEA and 2-AG, are generated by platelets and macrophages during septic-, haemorrhagic-, and shock-induced hypotension through activation of CB1 [ 103 ]. Specifically, AEA is considered to be a strong mediator of endotoxin-induced hypotension via activation of vascular CB1 [ 104 ] and is increased in the blood of endotoxic shock patients [ 105 ]. Also, preventing endotoxin-mediated upregulation of plasma AEA or 2-AG, by administering a CB1 inverse agonist (AM281), was beneficial in experimental animals, as it improved mortality associated with septic shock [ 106 ].…”

“…An early clinical trial (NCT00636766), which originated from findings in mouse models [ 104 ], examined the influence of rimonabant on atherosclerotic plaque stability and found the CB1 antagonist rimonabant promoted plaque regression and stability. Continuing this promising start, the 12-month long rimonabant in obesity (RIO) programs (Europe, Lipids, North America and Diabetes; NCT00386061) reported that rimonabant improved anthropometric data and modifiable cardiometabolic risk markers [ 158 ].…”