Related Experiment Video
Updated: Jun 11, 2026

Mitigation of Blood Borne Cell Attachment to Metal Implants through CD47-Derived Peptide Immobilization
Published on: December 3, 2020
Ascorbic acid infusion blunts CD40L upregulation in patients undergoing coronary stent
Pasquale Pignatelli1, Gaetano Tanzilli, Roberto Carnevale
1Prima Clinica Medica-Department of Experimental Medicine, University of Rome La Sapienza, Rome, Italy.
Insights
Ascorbic acid infusion effectively reduced oxidative stress and CD40L upregulation during coronary stenting. This antioxidant intervention offers a promising strategy to mitigate vascular event risks post-procedure.
Area of Science:
- Cardiology
- Biochemistry
- Vascular Biology
Background:
- CD40L upregulation post-coronary percutaneous coronary intervention is linked to vascular events.
- The precise mechanism driving CD40L upregulation remains unclear.
Purpose of the Study:
- To investigate the potential of ascorbic acid to reduce oxidative stress and CD40L upregulation during stenting.
- To explore the role of oxidative stress in CD40L upregulation in this context.
Main Methods:
- A randomized trial involving 56 patients undergoing elective coronary stenting.
- Intravenous ascorbic acid or placebo infusion was administered.
- Measurements included platelet CD40L, soluble CD40L, and 8-hydroxy-2'-deoxyguanosine (oxidative stress marker) pre- and post-stenting, with in vitro studies on platelet response to anoxia-reoxygenation.
Main Results:
- Placebo group showed increased platelet CD40L, soluble CD40L, and oxidative stress markers.
- Ascorbic acid group exhibited no change in soluble CD40L or platelet CD40L but a decrease in oxidative stress markers.
- Ascorbic acid significantly lowered soluble CD40L, platelet CD40L, and oxidative stress markers compared to placebo.
- In vitro, ascorbic acid inhibited reactive oxidant species and CD40L upregulation in platelets exposed to anoxia-reoxygenation.
Conclusions:
- Coronary stenting leads to CD40L upregulation.
- Oxidative stress is a likely mediator of this CD40L upregulation.
- Ascorbic acid demonstrates potential in mitigating these procedural effects.
Objectives:
To reduce the increase of oxidative stress and the upregulation of CD40L during stenting procedure using ascorbic acid infusion.
Background:
CD40L upregulation occurring after coronary percutaneous coronary intervention predicts vascular events but the underlying mechanism is still unclear.
Methods:
Fifty-six patients undergoing elective coronary stenting were randomly allocated to intravenous infusion of the antioxidant ascorbic acid or placebo. Platelet CD40L and plasma levels of soluble CD40L and of 8-hydroxy-2'-deoxyguanosine, a marker of oxidative stress, were measured before and after coronary stenting. In vitro study was also done to measure reactive oxidant species and CD40L expression in platelets exposed to anoxia-reoxygenation.
Results:
Placebo-treated patients showed a significant increase of platelet CD40L, soluble CD40L and 8-hydroxy-2'-deoxyguanosine compared to baseline values. Patients given ascorbic acid showed no change of soluble CD40L and platelet CD40L but a significant decrease of 8-hydroxy-2'-deoxyguanosine. After 60 and 120 min, soluble CD40L, platelet CD40L and 8-hydroxy-2'-deoxyguanosine were significantly lower in the ascorbic acid-treated group compared to the placebo-treated one. A significant correlation between platelet CD40L and soluble CD40L and between soluble CD40L and 8-hydroxy-2'-deoxyguanosine was observed. Platelets, in vitro exposed to anoxia-reoxygenation, had a burst of ROS and an upregulation of CD40L that were inhibited by ascorbic acid or apocynin, an inhibitor of NADPH oxidase.
Conclusions:
This study shows that in patients undergoing coronary stenting CD40L is upregulated with a mechanism which is likely mediated by oxidative stress.
Related Concept Videos
Coronary Artery Disease IV: Preventive Measures
Acute Coronary Syndrome III: Diagnostic Studies
Acute Coronary Syndrome I: Introduction
Atherosclerosis III: Management
Coronary Artery Disease I: Introduction
Angina IV: Management
