Choline induced cardiac dysfunction by inhibiting the production of endogenous hydrogen sulfide in spontaneously hypertensive rats
Language English Country Czech Republic Media print
Document type Journal Article
PubMed
38215059
PubMed Central
PMC10805251
DOI
10.33549/physiolres.935075
PII: 935075
Knihovny.cz E-resources
- MeSH
- Ventricular Function, Left MeSH
- Hypertension * chemically induced MeSH
- Collagen MeSH
- Rats MeSH
- Heart Diseases * MeSH
- Rats, Inbred SHR MeSH
- Rats, Inbred WKY MeSH
- bcl-2-Associated X Protein MeSH
- Hydrogen Sulfide * MeSH
- Sulfides * MeSH
- Stroke Volume MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- Collagen MeSH
- bcl-2-Associated X Protein MeSH
- sodium bisulfide MeSH Browser
- Hydrogen Sulfide * MeSH
- Sulfides * MeSH
To investigate the exact effects of dietary choline on hypertensive heart disease (HHD) and explore the potential mechanisms, male spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY) were randomly divided into five groups as follows: WKY group, WKY + Choline group, SHR group, SHR + Choline group, and SHR + Choline + NaHS group. In choline treatment groups, rats were fed with 1.3% (w/v) choline in the drinking water for 3 months. The rats in the SHR + Choline + NaHS group were intraperitoneally injected with NaHS (100 micromol/kg/day, a hydrogen sulfide (H2S) donor) for 3 months. After 3 months, left ventricular ejection fraction (LVEF) and fractional shortening (LVFS), the indicators of cardiac function measured by echocardiography, were increased significantly in SHR as compared to WKY, although there was no significant difference in collagen volumes and Bax/Bcl-2 ratio between the two groups, indicating the early stage of cardiac hypertrophy. There was a significant decrease in LVEF and LVFS and an increase in collagen volumes and Bax/Bcl-2 ratio in SHR fed with choline, meanwhile, plasma H2S levels were significantly decreased significantly in SHR fed with choline accompanying by the decrease of cystathionine-gamma-lyase (CSE) activity. Three months of NaHS significantly increased plasma H2S levels, ameliorated cardiac dysfunction and inhibited cardiac fibrosis and apoptosis in SHR fed with choline. In conclusion, choline aggravated cardiac dysfunction in HHD through inhibiting the production of endogenous H2S, which was reversed by supplementation of exogenous H2S donor.
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