ABC | Volume 111, Nº4, Octuber 2018

Original Article Yang et al ApoJ in neointimal hyperplasia Arq Bras Cardiol. 2018; 111(4):562-568 Figure 4 – Western blotting of apolipoprotein J (Apo J) protein levels 1 week (w), 2 weeks, 3 weeks and 4 weeks after balloon injury of rat carotid arteries. 3 2 1 0 Control Control Model Model Statin intervention Statin intervention 1W 1W 2W 2W 3W 3W 4W 4W Relative protein level (normalized to β-actin) Apo J Apo J Apo J Apo J β-actin β-actin β-actin β-actin Table 3 – Relative (2-ΔΔCt) levels of apolipoprotein J mRNA Time points Control group Model group Statin intervention group t * p # n 2-ΔΔCt n 2-ΔΔCt n 2-ΔΔCt 1 5 0.958 ± 0.251 5 0.641 ± 0.296 6 1.275 ± 0.468 a 4.212 0.039 2 5 0.948 ± 0.090 4 7.804 ± 1.328 a▲ 6 10.040 ± 2.086 ∆b 52.279 < 0.001 3 5 1.004 ± 0.196 4 8.011 ± 2.306 aβ 6 7.327 ± 2.869 ∆ * β 15.31 < 0.001 4 5 1.048 ± 0.349 4 3.429 ± 1.119 abcθ 6 2.413 ± 0.492 *#θ 14.212 0.001 F $ 0.182 29.266 31.336 P # 0.907 < 0.001 < 0.001 * t value was calculated using independent-samples t test to compare the difference between two groups. $ F value was calculated using one-way ANOVA (analysis of variance) to compare the difference among the four groups. # p value (probability value) < 0.05 is considered to be statistically significant. In-stent restenosis after interventional procedures has become one of the most urgent problems to be solved worldwide. Rosuvastatin, a potent hydroxymethylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, has been reported to reduce neointimal thickening after vascular endothelial injury in rats 13 In the present study, the rats in the intervention group received intragastric administration of rosuvastatin (10mg/kg/d). In accordance with other studies, 22-24 we found that rosuvastatin significantly reduced the neointima formation. It has been reported that secreted isoform of Apo J (sCLU) could inhibit the proliferation and migration of VSMCs. 12,25 Kim et al. 12 also found that Apo J could significantly inhibit neointimal hyperplasia using adenovirus-mediated overexpression of Apo J in rats. In the present study, we found that the mRNA and protein levels of ApoJ in carotid arteries were significantly upregulated after rosuvastatin administration as compared with the model group. Moreover, Apo J reached a maximum at week 2 after rosuvastatin administration, and that was earlier than themodel groupwhich reached peak expression at the third week. These results suggest that rosuvastatin may increase the level of Apo J in the balloon‑injured carotid arteries, which indirectly indicates a protective role of Apo J against restenosis after balloon-injury in rats. Conclusion Our results showed that Apo J served as an acutephase reactant after balloon-injury in rat carotid arteries. Rosuvastatin may reduce the neointima formation through further up‑regulation of Apo J. Our findings suggest that Apo J exerts a protective role against restenosis after balloon-injury in rats. Acknowledgements We greatly appreciate the help of Tianjin Cardiovascular Disease Research Institute on the animal experiment. Author contributions Conception and design of the research and Writing of the manuscript: Yang N, Qin Q; Acquisition of data: Yang N, Dong B, Yang J, Li Y, Kou L, Liu Y; Analysis and interpretation of the data: Yang N, Dong B, Yang J, Li Y, Kou L; Statistical 566