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Published on: October 15, 2010
Protective effects of cariporide on endothelial dysfunction induced by homocysteine
Shujin Wu1, Xiang Gao, Shehua Yang
1Department of Pharmacy, Gan Su Province Hospital, Lan Zhou, China.
Insights
Inhibiting the Na+/H+ exchanger (NHE) protects against homocysteine-induced endothelial dysfunction by reducing oxidative stress and inflammation. Cariporide treatment improved blood vessel function and lowered inflammatory markers.
Area of Science:
- Cardiovascular Science
- Pharmacology
Background:
- Homocysteine (Hcy) contributes to endothelial dysfunction.
- Intracellular calcium (Ca2+) and Na+/H+ exchanger (NHE) play key roles in Hcy-induced cardiovascular disease.
Purpose of the Study:
- To investigate the protective effects of NHE inhibition on Hcy-induced endothelial dysfunction.
- To explore the underlying mechanisms of cariporide's protective action.
Main Methods:
- Acetylcholine-induced endothelium-dependent relaxation (EDR) and biochemical parameters were assessed in rat aorta.
- Reactive oxygen species (ROS) and NF-κB pathway activation were analyzed.
Main Results:
- Cariporide significantly preserved EDR and enhanced nitric oxide (NO) release in Hcy-treated rats.
- Cariporide reduced ROS production, inhibited NF-κB activation, and decreased inflammatory markers (TNF-α, ICAM-1).
Conclusions:
- NHE inhibition by cariporide offers protection against Hcy-induced endothelial dysfunction.
- Mechanisms involve reducing oxidative stress and inflammatory injury via the NF-κB pathway.
Aims:
Recent studies have reported that intracellular calcium (Ca(2+)) mobilization is involved in homocysteine (Hcy)-induced endothelial dysfunction and the Na(+)/H(+) exchanger (NHE) is responsible for an increase in the intracellular Ca(2+) concentration in cardiovascular disease. We hypothesized that inhibition of the NHE had protective effects on Hcy-induced endothelial dysfunction.
Methods:
Acetylcholine-induced endothelium-dependent relaxation (EDR) and biochemical parameters were measured in the rat isolated aorta. The level of reactive oxygen species (ROS) was designed by a specific fluorescent probe. The phosphorylation of the nuclear factor-κB (NF-κB) system was studied by Western blot.
Results:
Cariporide significantly prevented Hcy-impaired EDR and increased nitric oxide (NO) release; endothelial NO synthase activity simultaneously decreased ROS production. We also found that cariporide blocked Hcy-induced NF-κB activation and inhibitor-κB degradation, thus inhibiting the production of tumor necrosis factor-α and intercellular adhesion molecule-1.
Conclusions:
The mechanisms of protective effects of cariporide may be related to the inhibition of NHE and the decrease in oxidative stress and inflammatory injury.
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