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Does ovariectomy impact oxidative stress in the right ventricle of female rats with monocrotaline-induced pulmonary arterial hypertension?
Does ovariectomy impact oxidative stress in the right ventricle of female rats with monocrotaline-induced pulmonary arterial hypertension?
In a rat model of monocrotaline-induced pulmonary arterial hypertension, ovariectomy increases hemoxygenase-1 and thioredoxin-1 expression, potentially modulating oxidative stress and attenuating right ventricular remodeling.
Ovariectomy may impair RV antioxidant defenses in experimental PAH; leaves open estrogen modulation's relevance to human right ventricular oxidative stress.
The aim of this study was to evaluate the impact of ovariectomy on oxidative stress in the right ventricle (RV) of female rats with pulmonary arterial hypertension (PAH) induced by monocrotaline (MCT). Rats were divided into 4 groups (n = 6 per group): sham (S), sham + MCT (SM), ovariectomized (O), and ovariectomized + MCT (OM). MCT (60 mg·kg −1 i.p.) was injected 1 week after ovariectomy or sham surgery. Three weeks later, echocardiographic analysis and RV catheterisation were performed. RV morphometric, biochemical, and protein expression analysis through Western blotting were done. MCT promoted a slight increase in pulmonary artery pressure, without differences between the SM and OM groups, but did not induce RV hypertrophy. RV hydrogen peroxide increased in the MCT groups, but SOD, CAT, and GPx activities were also enhanced. Non-classical antioxidant defenses diminished in ovariectomized groups, probably due to a decrease in the nuclear factor Nrf2. Hemoxygenase-1 and thioredoxin-1 protein expression was increased in the OM group compared with SM, being accompanied by an elevation in the estrogen receptor β (ER-β). Hemoxygenase-1 and thioredoxin-1 may be involved in the modulation of oxidative stress in the OM group, and this could be responsible for attenuation of PAH and RV remodeling.
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Siqueira et al. (2017) studied this question.
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