Abstract:

This study aims to explore the effect and mechanism of frankincense essential oil (FEO) on cardiac hypertrophy in rats based on NOD-like receptor protein 3 (NLRP3) inflammasome pathway. The ingredients of FEO were determined by gas chromatography-mass spectrometry. Cardiomyocytes were pretreated with 0.225 μg/mL FEO for 1 h followed by 10 µmol/L isoproterenol (ISO) treatment for 24 h. The effects of FEO on ISO-induced cardiomyocyte surface area, hypertrophy-related fetal gene expressions, the release of lactate dehydrogenase (LDH) and NLRP3 inflammasome-related gene and protein expressions were determined. Rats were intragastrically treated with FEO (50 or 100 mg/kg) for four weeks after undergoing coronary artery ligation (CAL) surgery to induce cardiac hypertrophy model. The heart weight, left ventricular weight, cardiomyocyte cross-sectional area, hypertrophy-related fetal gene expressions, NLRP3 inflammasome-related gene and protein expressions, and serum LDH content were measured. The results showed that FEO could significantly inhibit ISO-induced cardiomyocyte hypertrophy, reduce LDH release, and inhibit the expressions of NLRP3 inflammasome-related gene and protein. CAL surgery induced cardiac hypertrophy in rats as shown by increases in heart weight, left ventricular weight, and cardiomyocyte cross-sectional area, as well as upregulation of fetal gene expression. Additionally, CAL surgery also induced NLRP3 inflammasome activation as evidenced by increased serum LDH content and upregulated expressions of NLRP3 inflammasome-related gene and protein. FEO inhibited these above changes induced by CAL. Therefore, FEO can improve cardiac hypertrophy in rats by inhibiting NLRP3 inflammasome.

Key words: cardiac hypertrophy, coronary artery ligation, frankincense essential oil, NLRP3 inflammasome