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A Slow Hydrogen Sulfide Donor GYY-4137 Partially Improves Vascular Function in Spontaneously Hypertensive Rats Fed a
Basak G Aydemir1, Andrea Berenyiova1,2, Martina Cebova1,2
1Institute of Normal and Pathological Physiology, Centre of Experimental Medicine, Slovak Academy of Sciences, 841 04 Bratislava, Slovakia.
Summary
A slow-releasing hydrogen sulfide (H₂S) donor, GYY-4137, partially improved metabolic changes and cardiovascular function in rats fed a high-fat diet. This intervention restored nitric oxide (NO) signaling and reduced inflammation, offering potential therapeutic benefits.
Area of Science:
- Cardiovascular Research
- Metabolic Syndrome Studies
- Pharmacology
Background:
- Metabolic syndrome, driven by high-fat diet (HFD) intake, is a major global mortality cause.
- Cardiovascular disorders linked to metabolic syndrome necessitate novel therapeutic interventions.
Purpose of the Study:
- To investigate the therapeutic potential of GYY-4137, a slow-releasing hydrogen sulfide (H₂S) donor.
- To evaluate the effects of GYY-4137 on cardiovascular and metabolic parameters in a rat model of HFD-induced metabolic changes.
Main Methods:
- Male spontaneously hypertensive rats (SHRs) were fed an HFD for 8 weeks.
- Rats were treated with GYY-4137 for 3 weeks to assess effects on blood pressure, cardiac function, adiposity, plasma markers, and vascular reactivity.
- Vascular function of thoracic aortas (TAs) and mesenteric arteries (MAs) was analyzed.
Main Results:
- HFD induced cardiac remodeling, increased adiposity, and impaired vascular contractility.
- HFD altered nitric oxide (NO) signaling pathways and increased inflammation markers (inducible NOS, TNFα, chemerin).
- GYY-4137 treatment reduced systolic blood pressure, improved vascular relaxation and contractility, restored NO signaling, and decreased inflammation markers.
Conclusions:
- A slow H₂S-releasing donor (GYY-4137) can partially ameliorate HFD-induced metabolic dysfunction in hypertension.
- GYY-4137 demonstrates beneficial vasoactive effects by restoring NO signaling and suppressing inflammation.

