ABSTRACT
Kawasaki disease (KD), a febrile systemic vasculitis in infants associated with coronary aneurysm, is a major cause of cardiac sequelae such as myocardial infarction (MI) and sudden death. These events are caused by coronary stenosis due to intimal proliferation or thrombotic formation; however, histological evaluation is limited to autopsy cases of human KD. We therefore investigated the histological features of coronary artery (CA) stenosis in mice induced by Lactobacillus casei cell wall extract (LCWE). LCWE-induced coronary inflammation gradually progressed in a time-dependent manner and expanded to all layers of the vessel wall over 28 days. In addition, frequent elastin degradation was observed and abundant α-smooth muscle actin (SMA)-positive vascular smooth muscle cells (VSMCs) infiltrated into the intima. Furthermore, most VSMCs were positive for proliferating cell nuclear antigen (PCNA) following staining, suggesting that VSMCs likely exhibited a proliferative phenotype. In conclusion, we show a novel mouse model of coronary stenosis induced by LCWE that is characterized by coronary stenosis with severe coronary vasculitis and elastin degradation. In addition, VSMC proliferation plays an important role in the formation of coronary stenosis. This model is an appropriate model of KD coronary stenosis.
Subject(s)
Coronary Stenosis , Disease Models, Animal , Lacticaseibacillus casei , Mucocutaneous Lymph Node Syndrome , Animals , MiceABSTRACT
@#ObjectiveTo observe the effects of all-transretinoic acid (ATRA) on cell apoptosis and p53 expression in rabbits' carotid atherosclerosis. Methods40 New Zealand rabbits were randomly divided 4 groups: normal group (NOR), control group (CON), surgery group (SUR) and treat group (TRE). Each group was fed with high cholesterol forage. The SUR and TRE groups were made up carotid atherosclerotic model by air desiccation injury after 2 weeks. The TRE group was fed with ATRA before surgery. On the 2nd and 4th week after operation, the target vessel was taken out. The intima hyperplasia was observed by microscopy through HE staining. Cell apoptosis was determined by TUNEL staining and p53 was observed by immunohistochemistry staining. ResultsOn the 4th week, the area of neointima in SUR, TRE and CON were (0.389±0.021) mm2, (0.113±0.038) mm2, (0.069±0.016) mm2 (P<0.01). The positive cells rate of TUNEL (8.40±0.45)% and p53 (3.02±0.38)% in TRE were higher than those of SUR (8.59±0.42)% and (2.23±0.29)%, respectively (P<0.01). ConclusionATRA may induce cell apoptosis in atherosclerotic plaque and inhibit the proliferation of intima associated with p53 in vessel injury.
ABSTRACT
Background The ubiquitin-proteasome pathway(UPP)involves 80%-90% degradation of all in- tracellular proteins.Both ubiquitin and rat component 3 of proteasome(RC3)are hence considered to be central me- diators for cell biology.Objective To evaluate the effect of simvastatin on neointimal hyperplasia and the expres- sion of ubiquitin and rat component 3 of proteasome(RC3)after balloon injury in carotid artery.Methods Thirty- two male SD rats were randomly to receive,low dose(0.4 mg/ng,n=8),or moderate(4 mg/ng,n=8),or high- dose(40 mg/ng,n=8)of simvastatin treatment for 28 days.Common carotid aortic artery was injuried rat ballon. The ratio of intima-media(I/M)thickness was determined.The expression level of ubiquitin and RC3 mRNA were assessed by RT-PCR.The expression level of ubiquitin protein was examined with immunohistochemistry. Results Simvastatin inhibited the expression of ubiquitin and RC3 mRNA and ubiquitin protein in dose dependent manner.The intima-media ratio(-50.2 %)and the expression of ubiquitin(-60.3 %)and RC3 mRNA and ubiq- uitin protein(-60.5 %)was reduced by the high dose simvastatin [40 mg/(kg?d)](P
ABSTRACT
Objective:To observe the effect of Radix Paeoniae Rubra on intimal proliferation,activating of angiotensin Ⅱ(AgⅡ) and expression of Mitogen-activated protein kinase phosphatase-1(MKP-1) after carotid artery balloon injury in cholesterol-fed rabbits.Methods: Male rabbits were randomly divided into Radix Paeoniae Rubra(PPR) groups: high dose group(75、50、25g.kg-1.d-1;n=8),middle dose group(2g.kg-1.d-1),low dose group(1g.kg-1.d-1;n=8) and control group.Both groups received high fat forage(2% cholesterol + 5% lard).Balloon injury of carotid artery was performed.Carotid artery were harvested at the end of 10 weeks.Expression level of AgⅡwas measured by radioimmunoassay.MKP-1 expression was determined by RT-PCR.Immunohistochemical staining and morphological detection were adopted.Results: Compare with control group,expression of AgⅡ decreased obviously(P
ABSTRACT
Objective To study the effects of Batroxobin( BX) on the intimal proliferation of graft veins. Methods In this study 25 dogs were selected and evenly divided into experimental group, control group and sham operation group. In experiment and control group, a segment of auto- femoral vein were grafted into femoral artery by clean microsurgery technique. In experimental group, BX was given at the dosage of 0. 1 BU/kg, dayly?2 preoperatively, and once a day for consecutive 6 days postoperatively. Plasma NO, ET was determined in the three groups. Computer image analysis system was applied to calculate the thickness of neointima and media in the vein grafts, immunohistochemistry was used to identify PCNA and C-myc. Result The experimental group had a higher level of NO and lower level of ET compared with control group and sham operation group(P 0. 05 ). The PCNA expression in experimental group was statistically different from that of the control group(P