Key result
Naringenin inhibits high glucose-induced cardiomyocyte hypertrophy via joint activation of EETs and PPARs.
Why the study?
Cardiac hypertrophy is a key pathological process in diabetic cardiomyopathy, but the effect of naringenin on cardiomyocyte hypertrophy under diabetic conditions remains unclear.
Does naringenin prevent high glucose-induced cardiomyocyte hypertrophy in H9c2 cells?
Does naringenin prevent high glucose-induced cardiomyocyte hypertrophy in H9c2 cells?
p-value: p=<0.05
Naringenin attenuates high glucose-induced cardiomyocyte hypertrophy in vitro via a mechanism involving the activation of EETs and PPARs.
May support naringenin investigation in diabetic cardiomyopathy models; leaves open translation from in vitro findings to clinical use.
BACKGROUND: Cardiac hypertrophy is a key pathological process in the context of diabetic cardiomyopathy. Naringenin exhibits multiple pharmacological activities, but the effect of naringenin on cardiomyocyte hypertrophy under diabetic conditions is still far from clear. METHODS: Cardiomyocyte hypertrophy was induced by high glucose (HG, glucose at 25.5 mmol/L) in H9c2 cells, which was determined by cell surface area, protein content and atrial natriuretic factor (ANF) mRNA expression. The effect of naringenin on cardiomyocyte hypertrophy was observed and its mechanisms were investigated by administration with various inhibitors on epoxyeicosatrienoic acids (EETs)/peroxisome proliferator-activated receptors (PPARs). The level of 14,15-EET was measured by ELISA. The mRNA and protein expressions were detected by qRT-PCR or Western blot, respectively. RESULTS: Naringenin (0.1, 1, 10 μmol/L) inhibited cardiomyocyte hypertrophy in a concentration-dependent manner (P < 0.05), up-regulated the expressions of PPARα, PPARβ, PPARγ and CYP2J3 (P < 0.05), and increased the level of 14,15-EET (P < 0.05). PPOH, a CYP2J3 inhibitor, blocked the naringenin-mediated improvement of myocardial hypertrophy (P < 0.01), and abolished the up-regulation of PPARs expressions (P < 0.01). Meanwhile, MK886, a PPARα antagonist, GSK0660, a PPARβ antagonist, and GW9662, a PPARγ antagonist, reversed the protection of naringenin on cardiomyocytes (P < 0.05), and abrogated the up-regulation of CYP2J3-EET produced by naringenin (P < 0.05). CONCLUSIONS: Activation of EETs and PPARs function together may be contributed to the anti-hypertrophic effect of naringenin in H9c2 cells under high glucose condition.
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Zhang et al. (2018) studied High glucose-induced cardiomyocyte hypertrophy. Naringenin vs. High glucose control was evaluated on Cardiomyocyte hypertrophy (cell surface area, protein content, and ANF mRNA expression) (p=<0.05). Naringenin inhibited high glucose-induced cardiomyocyte hypertrophy in a concentration-dependent manner (P<0.05), an effect mediated by the joint activation of EETs and PPARs.
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