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[Effect of FK506 and CsA on vascular endothelium of hyperlipidemic rats]
Wei Wang1, Kai-xuan Yang, Peng Zhang
1Department of Pathology, West China Second Hospital, Sichuan, Chengdu 610041, China.
Insights
Ciclosporin A (CsA) damages hyperlipidemic rat vascular endothelium by increasing ROS and CRP, while inhibiting VEGF and DAF. FK506 showed no adverse effects on the vascular endothelium.
Area of Science:
- Pharmacology
- Cardiovascular Biology
- Immunology
Background:
- Hyperlipidemia poses risks to vascular health.
- Understanding drug effects on vascular endothelium is crucial.
Purpose of the Study:
- To investigate the impact of ciclosporin A (CsA) and FK506 on vascular endothelium in hyperlipidemic rats.
Main Methods:
- Established a hyperlipidemic rat model.
- Assessed vascular endothelium injury after CsA/FK506 administration.
- Measured VEGF, DAF, CRP mRNA/protein expression and serum ROS levels.
Main Results:
- CsA significantly injured vascular endothelium, unlike FK506.
- CsA decreased vascular endothelium growth factor (VEGF) and decay-accelerating factor (DAF) expression.
- CsA increased C-reactive protein (CRP) and reactive oxygen species (ROS) levels.
Conclusions:
- CsA damages hyperlipidemic rat vascular endothelium via complement system activation, involving VEGF/DAF and ROS/CRP pathways.
- FK506 demonstrated no impact on these pathways or ROS/CRP expression.
Objective:
To observe the influence of ciclosporin A (CsA) or/and FK506 on vascular endothelium of hyperlipidemic rats.
Methods:
Hyperlipidemic rat model was established as previously described. The injury of vascular endothelium of these rats was observed after stimulation with FK506 or/and CsA. The mRNA transcription and protein expression of the vascular endothelium growth factor (VEGF), decay-accelerating factor (DAF) and C reactive protein (CRP) in vascular endothelium of rats were measured. The serum reactive oxygen species (ROS) was detected.
Results:
Compared with FK506, CsA was more likely to cause injury of vascular endothelium, damaging the integrity of endothelium of hyperlipidemic rats. CsA inhibited the expression of VEGF and the complement inhibitor DAF and increased the expression of CRP of vascular endothelial cells. CsA also up-regulated the serum level of ROS. FK506 showed no such impacts.
Conclusion:
CsA can damage vascular endothelium of hyperlipidemic rats by activating the complement system induced by VEGF/DAF and ROS/CRP pathway. FK506 has no influence on the VEGF/DAF pathway and the expression of ROS/CRP.
