Key result
Hydroxysafflor yellow A significantly reduced haemodynamic changes, right ventricular hypertrophy, inflammation, and oxidative stress in rats with monocrotaline-induced pulmonary hypertension.
Why the study?
Does hydroxysafflor yellow A (HSYA) improve established monocrotaline-induced pulmonary arterial hypertension in rats?
Does hydroxysafflor yellow A (HSYA) improve established monocrotaline-induced pulmonary arterial hypertension in rats?
Hydroxysafflor yellow A (HSYA) attenuates monocrotaline-induced pulmonary arterial hypertension in rats, likely via suppression of inflammation and oxidative stress.
OBJECTIVE: To evaluate the beneficial effects of hydroxysafflor yellow A (HSYA) on monocrotaline (MCT)-induced pulmonary arterial hypertension (PAH) in rats, and to investigate the main pathophysiological mechanism of HSYA in preventing development of MCT-induced PAH. METHODS: Four groups (control, control with HSYA treatment, MCT-exposed, and MCT-exposed with HSYA treatment) were evaluated at day 28 following MCT exposure. Haemodynamic measurements, right ventricular hypertrophy, morphometry, inflammatory cytokines and oxidant expression were assessed. RESULTS: HSYA significantly reduced haemodynamic changes, right ventricular hypertrophy and morphometric changes induced by exposure to MCT. HYSA also suppressed MCT-induced inflammation and oxidative stress in rat pulmonary tissue. CONCLUSIONS: Experimental MCT-induced PAH may be reduced by HSYA treatment, and the mechanism may involve suppression of inflammation and oxidative stress.
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Han et al. (2016) studied Monocrotaline-induced pulmonary arterial hypertension. Hydroxysafflor yellow A (HSYA) vs. Control (no HSYA treatment) was evaluated on Haemodynamic measurements, right ventricular hypertrophy, morphometry, inflammatory cytokines and oxidant expression. Hydroxysafflor yellow A significantly reduced haemodynamic changes, right ventricular hypertrophy, inflammation, and oxidative stress in rats with monocrotaline-induced pulmonary hypertension.
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