ArticleIranian journal of basic medical sciences2026
Nerolidol attenuates cardiac hypertrophy and fibrosis in mice: Modulation of collagen type I, apoptotic and endothelial gene expression.
Article in Iranian journal of basic medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: 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 8 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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