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Effect of curcumin on the adhesion of platelets to brain microvascular endothelial cells in vitro
Li Zhang1, Zhen-lun Gu, Zheng-hong Qin
1Department of Pharmacology and Laboratory of Aging and Nervous Diseases, Soochow University School of Medicine, Suzhou 215123, China.
Insights
Curcumin effectively inhibits platelet adhesion to brain microvascular endothelial cells (BMECs). This effect is linked to reduced expression of key adhesion molecules like P-selectin and GPIIb/IIIa.
Area of Science:
- Biomedical Science
- Molecular Biology
- Cell Biology
Background:
- Platelet adhesion to brain microvascular endothelial cells (BMECs) plays a role in neuroinflammation and cerebrovascular diseases.
- Understanding molecular mechanisms that regulate this interaction is crucial for developing therapeutic strategies.
Purpose of the Study:
- To investigate the inhibitory effect of curcumin on platelet adhesion to BMECs in vitro.
- To elucidate the molecular targets of curcumin in this process.
Main Methods:
- In vitro co-culture of [3H]adenine-labeled platelets with BMECs.
- Quantification of platelet adhesion using liquid scintillation spectroscopy.
- Analysis of cell surface marker expression (P-selectin, GPIIb/IIIa, E-selectin) via flow cytometry and Western blotting.
- Assessment of P-selectin mRNA levels in BMECs using RT-PCR.
Main Results:
- Curcumin significantly inhibited thrombin-activated platelet adhesion to BMECs in a dose-dependent manner.
- Curcumin treatment reduced the expression of P-selectin on activated platelets and P-selectin and E-selectin on TNF-alpha-stimulated BMECs.
- Curcumin also inhibited the upregulation of glycoprotein IIb/IIIa on activated platelets.
Conclusions:
- Curcumin demonstrates potent inhibitory effects on platelet-BMEC adhesion.
- The anti-adhesive property of curcumin is associated with the downregulation of key adhesion molecules, including P-selectin, E-selectin, and GPIIb/IIIa.
- These findings suggest curcumin as a potential therapeutic agent for conditions involving platelet-endothelial cell interactions in the brain.
Aim:
To determine whether curcumin prevents the adhesion of platelets to brain microvascular endothelial cells (BMECs) cultured in vitro.
Methods:
[3H]Adenine- labeled platelets were incubated with BMECs to investigate the role of curcumin in the adhesion of platelets to BMECs. The number of platelets adhering to the BMECs monolayer was determined by liquid scintillation spectroscopy. The thrombin-induced expression of platelets P-selectin, glycoprotein IIb (GPIIb), and glycoprotein IIIa (GPIIIa) on the cell surface, was measured by flow cytometry. P-selectin mRNA levels of BMECs were determined by RT-PCR. The TNF-alpha- induced expressions of P-selectin and E-selectin on the surface of BMECs were determined by Western blotting.
Results:
The adhesion between thrombin-activated platelets and normal BMECs, and that of TNF-alpha-activated BMECs and normal platelets were significantly increased, and this increase could be inhibited by curcumin (30-240 micromol/L) in a concentration-dependant manner. The platelets activated with thrombin and BMECs stimulated by TNF-alpha demonstrated an upregulated expressions of P-selectin and E-selectin, and this increase, when pretreated with curcumin for 30 min, could be restrained dose dependently. Curcumin also inhibited the increase of the GPIIb/GPIIIa expression of thrombinactivated platelets in a concentration-dependent manner.
Conclusion:
Curcumin can inhibit the platelets to BMECs. This effect may be related to the decreased expressions of P-selectin, E-selectin, and GPIIb/GPIIIa on platelets and BMECs.
