| Background and objective: Restenosis is a main complication of coronary heart disease after percutaneous coronary intervention, largely because of the increasing expression of the growth and inflammation factors, and the triggering coagulation cascade after balloon injury. As a major component in tea polyphenols, epigallocatechin-3-gallate(EGCG)has been reported that it have the antiproliferative effects in vascular smooth muscle cells (VSMCs) by suppressing the expression of some growth factors and inducing the proliferated cell apoptosis in culture, but it is uncertain weather EGCG could inhibit restenosis or not after angioplasty in vitro. The study aim to investigate the effects of EGCG on vascular restenosis in rats after aorta balloon injury, and try to elucidate the mechanism of neointima formation by analysising the expressions of the growth factors on VSMCs and cell apoptosis in the neointima.Materials and Methods: The model of aorta injury was established by balloon catheter which induced endothelium denudation. 72 male SD rats were randomly divided into:①control group, which received only left common carotid ligation;②model group, which subjected left common carotid ligation and aorta injury by balloon catheter;③the low dose EGCG group, which underwent aorta injury and infused with 20mg/kg daily EGCG intragastrically;④high dose group, which was infused with 50mg/kg daily EGCG intragastrically after previous operation. All administration was given three days before operation and matching normal saline was infused to control and model groups until the end point of the experiment. The aorta of 9 randomly selected rats from each group were harvested on postoperative days 14 and 28 for H-E staining and vessel morphological detection; meanwhile, Masson trichrome staining was taken to estimate collagen fibers content in the neointima; further more, immunohistochemical staining was performed to measure the expression of proliferation cell nuclear antigen (PCNA), platelet-derived growth factor (PDGF)-BB, basic fibroblast growth factor (b-FGF), and transforming growth factor (TGF)-β1. Finally, VSMCs apoptosis level in the intima was gauged by TUNNEL staining.Result: There were 4 rats died of various causes such as infections and thrombosis, 68 rats were involved in the result analysis.①Neoformative intima in model group was increased in thickness (NT) and area (NA) markedly from aorta thoracica to the upper and lower vessel of the abdominal aorta and stenosis became evident gradually.②NT and NA to Low dose EGCG group were decreased since the postoperative day 14, and not significantly different from those of the model group (P＞0.05); while they were significantly decreased from the 28th day (P＜0.05). NT and NA of the high dose group were significantly decreased on the 14th and 28th days after aorta injury (P＜0.01).③Collage fibers content were increased in the model group both in the 14th and 28th day after operation, but were not affected by EGCG either in low dose or high dose.④Expression of PCNA, PDGF-BB, b-FGF and TGF-β1 were increased remarkably in the model group; low dose EGCG had no obvious inhibition to the expression of PCNA, PDGF-BB and b-FGF, while high dose EGCG significantly inhibited the expression of PCNA, PDGF-BB and b-FGF. EGCG had no effected on the expression of TGF-β1.⑤There was a lower rate of cell apoptosis in neointima of the model group than in the control group; but EGCG could greatly induced proliferating VSMCs apoptosis in the two doses at each time points, and the high dose group had higher apoptosis level than low dose group in the day 28(P＜0.05)。Conclusion: EGCG could dose-dependently attenuate the arterial stenosis in aorta injuried rats, largely for inhibiting the expressions of PDGF-BB and bFGF and inducing the apoptosis of VSMCs.
|
PDF Full Text Request