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Updated: May 12, 2026

An In Vivo Estrogen Deficiency Mouse Model for Screening Exogenous Estrogen Treatments of Cardiovascular Dysfunction After Menopause
Published on: August 13, 2019
Estrogens increase cystathionine-γ-lyase expression and decrease inflammation and oxidative stress in the myocardium
Xiaoyan Zhu1, Zhiping Tang, Binhai Cong
1From the 1Department of Physiology, Second Military Medical University, Shanghai, China; and 2School of Kinesiology, Key Laboratory of Exercise and Health Sciences of Ministry of Education, Shanghai University of Sport, Shanghai, China.
Estrogen (E2) boosts heart hydrogen sulfide (H2S) production by increasing cystathionine-γ-lyase (CSE) expression. This reduces oxidative stress and inflammation, suggesting a cardioprotective role for estrogens.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Biochemistry
Background:
- Hydrogen sulfide (H2S) is endogenously produced in the myocardium, primarily via cystathionine-γ-lyase (CSE), and exhibits cardioprotective properties.
- Estrogens, particularly 17β-estradiol (E2), are known to influence cardiovascular health, but their specific impact on myocardial H2S generation and related pathways requires elucidation.
Purpose of the Study:
- To investigate the effects of E2 on CSE expression and H2S generation within the myocardium.
- To determine the association between serum E2 levels and myocardial CSE activity and H2S production.
- To examine the relationship between E2/H2S levels and markers of oxidative stress and inflammation.
Main Methods:
- Ovariectomized rats were treated with E2 or vehicle for 12 weeks.
- Measurements included myocardial CSE expression, H2S generation, antioxidant capacity (GSH/GSSG ratio, T-AOC, SOD, CAT), and inflammatory markers (IL-6, TNF-α).
Main Results:
- E2 administration significantly increased myocardial CSE expression and H2S generation.
- Serum E2 levels positively correlated with H2S production and markers of antioxidant capacity (GSH/GSSG, T-AOC, SOD, CAT).
- E2 treatment and higher serum E2 levels were associated with reduced levels of proinflammatory cytokines (IL-6, TNF-α).
Conclusions:
- 17β-estradiol upregulates CSE expression and enhances endogenous H2S generation in the heart.
- These effects are linked to a reduction in oxidative stress and inflammation.
- Estrogens may confer cardioprotection by increasing myocardial H2S production via CSE pathway activation.
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