Key result
Nerolidol attenuates cardiac hypertrophy and fibrosis in mice by modulating apoptotic markers and up-regulating eNOS.
Why the study?
Cardiac hypertrophy is a major feature of cardiovascular disease and terpenes have known beneficial cardiovascular effects, prompting evaluation of the cardioprotective effects of the sesquiterpene alcohol nerolidol.
Does nerolidol reduce cardiac hypertrophy and fibrosis in an isoproterenol-induced mice model?
Does nerolidol reduce cardiac hypertrophy and fibrosis in an isoproterenol-induced mice model?
Nerolidol attenuates isoproterenol-induced cardiac hypertrophy and fibrosis in mice by modulating apoptotic, fibrotic, and endothelial gene expression.
Nerolidol merits further preclinical testing in cardiac models; leaves open any role in human hypertrophy or fibrosis.
Objective(s): Cardiac hypertrophy is a major pathological feature of cardiovascular disease worldwide. The beneficial effects of terpenes on cardiovascular diseases are well known. In the current study, the cardioprotective effects of nerolidol (NRD), a sesquiterpene alcohol, were evaluated using an isoproterenol (ISO) induced cardiac hypertrophy mice model. Materials and Methods: This study was performed by using the chronic subcutaneous infusion model of ISO. Male mice were administered NRD (100 mg/kg) orally for 7 days. On the 8th day with the continuation of NRD dosing, mice received subcutaneous (SC) with ISO (10 mg/kg) for the next 14 days. Cardiac functions, including ejection fraction, cardiac output, and fractional shortening were evaluated by trans-thoracic echocardiography, one day after the final treatment. Then, animals were euthanized and hearts were isolated. The mRNA and protein expressions of cardiac hypertrophy, apoptosis, and fibrosis markers in mice hearts were determined. Results: Results showed an increased heart-to-body weight ratio. NRD reduced cardiac hypertrophy by down-regulating the hypertrophic (ANP), apoptotic (Bax/Bcl-2), and fibrotic (Col1a1) markers and prevented cardiac remodeling by up-regulating expression of endothelial nitric oxide synthase (eNOS) and anti-apoptotic (Bcl-xL) protein compared to ISO-treated mice. Combining PCR and western blotting data results demonstrated that NRD reverted the ISO-induced cardiac hypertrophy. Conclusion: These findings suggest that NRD prevents ISO-induced cardiac hypertrophy possibly by elevating the levels of eNOS and Bcl-xL and reducing expression of hypertrophic, apoptotic, and fibrotic markers. Thus, NRD may be used to treat ISO-induced cardiac hypertrophy.
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Sadaf et al. (2026) studied Isoproterenol-induced cardiac hypertrophy. Nerolidol vs. Isoproterenol alone was evaluated on Cardiac hypertrophy, apoptosis, and fibrosis markers and cardiac functions. Nerolidol attenuated isoproterenol-induced cardiac hypertrophy and fibrosis in mice by down-regulating hypertrophic, apoptotic, and fibrotic markers and up-regulating eNOS and Bcl-xL.
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