The Effects Of CRP On The Expression Of PGI₂,PAI-1 In ECV304 Cells

Objective: To observe the possible effects of C-reactive protein(CRP) on the expression of prostaglandin I2 (PGI2) , Plasminogen Activator Inhibitor-1 (PAI-1) by ECV304 cells and assess the possible role in AS and acute coronary syndromes(ACS).Medthods: Through incubation of ECV304 cells with different concentration of CRP (0 mg/L, 25 mg/L, 50mg/L, 100mg/L) for 24 hours, to observe the dose effect of CRP in ECV304 cells. Through incubation of ECV304 cells with CRP (50mg/L) for different time (3 hours, 6 hours, 12 hours, 24 hours), to observe the time effect of CRP in ECV304 cells. measure the concentration of 6-keto-PGF1α, PAI-1 in cultural fluid by enzyme-linked immunosorbent assay (ELLISA). Group datas are mean±SD,through SPSS 11.0 software, datas are analyed by one-way ANOVA or t -test. Differences were considered significant at a value of P <0.05.Results: (l)Incubation of ECV304 cells with CRP results in a time- (6h VS 3h t =4.84,P =0.008; 12hVS 6h t =10.73, P =0.000; 24hVS 12ht =2.95, P =0.042) and dose-dependent (P =0.000) increase in secreted PAI-1 ; at 3 hours PAI-1 exceed control group (3h t = 3.37,P =0.028; 6h t =8.83, P =0.001; 12h t =13.86, P =0.000; 24h t =8.00, P =0.001)。 (2) Incubation of ECV304 cells with CRP results in dose-dependent(P =0.000) decrease in secreted PGI2;Incubation of ECV304 cells with CRP(50ug/ml) results in a time-dependent increase in secreted PGI2 in the first 12h (6h VS 3h t = 17.41, P =0.000; 12h VS 6h/ = 6.93,/> =0.002) and significantly decreased after 12 hours(f =3.23,? = 0.032); at 3 hours PGI2 exceed control group(/ =3.86, P =0.018) , no significant difference at 6 hours (/ =2.13, P =0.100)and decreased at 12 hours and 24 hours (121k 24h/ =10.87, 13.11, P =0.001).Conclusions: CRP induces the production of PAI-1 and quenches the production of PGI2 in ECV304 cells and has implications for angiospasm -. plaque rupture, thrombosis. These finds support the hypothesis that CRP may play a direct role in ACS and present a potential target for the treatment of AS and ACS.