Effects of hypertriglyceridemia and fenofibrate on CD40L expression in platelets / 中国病理生理杂志

ABSTRACT

AIM: To observe the effects of hypertriglyceridemia and fenofibrate on CD40L expression in platelets in vitro and in vivo. METHODS: In vivo experiments, according to its own strict standards, 20 patients were respectively selected for hypertriglyceridemia group and control group, before and after treatment of fenofibrate for hypertriglyceridemia patients. The CD40 ligand positive rates of platelets by flow cytometry and plasma soluble CD40 ligand by ELISA were examined under the same conditions as control group. The CD40L and sCD40L in each group were compared. In in vitro experiments, all 6 objects plasma was chosen in the same condition except for triglyceridemia, after the co-incubation of these plasma with the same healthy platelets was performed and the interference with wy14643, the CD40 ligand positive rate of platelets by flow cytometry and total platelets CD40 ligand protein content by Western blotting were examined under the same conditions in all objects. The CD40L positive rate and total CD40L content in each group were compared, respectively. RESULTS: The platelet CD40L positive rate and plasma sCD40L concentration in hypertriglyceridemia group were significant higher than those in control group (P<0.01). Followed the TG concentration decreased, the platelet CD40L positive rate and plasma sCD40L concentration decreased after the treatment of fenofibrate, the same as the total platelets CD40L content which was significant higher in hypertriglyceridemia group than that in control group in vitro (P<0.05). No effect of wy14643 on the total CD40L content expression was observed in vitro. CONCLUSION: Hypertriglyceridemia plasma stimulates immune-activation of platelets both in vitro and in vivo. sCD40L may mainly come from CD40L on platelet membrane. PPARα activator of fenofibrate may inhibit the immune-activation of platelets by reducing the concentration of plasma TG, but PPARα activator WY14643 cant inhibit the expression of CD40L and CD40L in vitro.