The cannabinoid CB1 receptor antagonist, rimonabant, protects against acute myocardial infarction.

作者: Shiang Y Lim , Sean M Davidson , Derek M Yellon , Christopher CT Smith , None

DOI: 10.1007/S00395-009-0034-2

关键词: CardiotoxicityEndocrinologyAdiponectinRimonabantCardioprotectionCannabinoidMedicineInfarctionInternal medicineCannabinoid receptorAntagonist

摘要: CB1 antagonism is associated with reduced doxorubicin-induced cardiotoxicity and decreased cerebrocortical infarction. Rimonabant, a selective receptor antagonist, was, before it was withdrawn, proposed as treatment for obesity reported to reduce cardiovascular risk by improving glucose lipid profiles raising adiponectin levels. The cardioprotective actions of rimonabant in 6-week-old C57BL/6J mice fed either high-fat (HFD) or standard diets (STD) 8 weeks were investigated. At 14 weeks, received (10 mg/kg/day, i.p.) vehicle 1 week then subjected an vivo acute myocardial influence on infarct size (IS) knockout (CB1−/−) wild-type (CB1+/+) also examined. that had been maintained STD HFD exhibited 4.3 21.4% reductions body weight following 7 days treatment. Rimonabant IS both (29.6 ± 3.5% vs. 49.8 ± 6.9% control, P   0.05), although significant seen CB1+/+ (IS, 48.9 ± 4.6% control 30.5 ± 3.1% rimonabant,  0.05). Serum cardiac levels unaltered HL-1 cell death not prevented 1 rimonabant. We conclude rimonabant-induced limitation may involve the receptor, necessarily receptors, unrelated loss altered synthesis.

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