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OBJECTIVE@#To determine the effects of hawthorn extract on serum lipid levels, pathological changes in aortic atherosclerosis plaque, inflammatory factors, and apoptosis-related protein and mRNA expression in apolipoprotein E gene knockout (ApoE) mice.@*METHODS@#Thirty-six ApoE mice were fed with a high-fat diet starting at the age of 8 weeks. Mice were randomly divided into 3 groups by a random number table including model group, hawthorn extract group, and simvastatin group, 12 mice in each group. Twelve 8-week-old C57BL/6 mice were fed a basic diet and served as control. The mice in the control and model groups were administered 0.2 mL saline daily, the mice in the hawthorn extract and simvastatin groups were administered with 50 mg/kg hawthorn extract or 5 mg/kg simvastatin daily for 16 weeks. After 16 weeks, plasma lipids including total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) were determined by an enzymatic assay. Aortic atherosclerotic lesions were observed by light microscopy, scanning and transmission electron microscopy, respectively. Plasma levels of monocyte chemoattractant protein-1 (MCP-1), interleukin-1β (IL-1β), adiponectin (APN), and hypersensitive C-reactive protein (hs-CRP) were measured by enzyme-linked immunosorbent assay (ELISA). Protein and mRNA expressions of Bax and Bcl-2 in the aorta were assessed by Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR), respectively.@*RESULTS@#Compared to the control group, the plasma levels of TC, TG and LDL-C were significantly increased and HDL-C were significantly decreased in the model group (P<0.01). Compared to the model group, treatment with hawthorn extract significantly decreased the plasma levels of TC, TG, and LDL-C and increased the plasma level of HDL-C in ApoE mice (P<0.01). The levels of MCP-1, IL-1ß, and hs-CRP in the model group were significantly increased and APN was significantly decreased compared with the control group (P<0.01). Compared to the model group, treatment with hawthorn extract decreased the levels of MCP-1, IL-1ß, and hs-CRP and increased the APN level (P<0.01). Compared to the control group, the protein and mRNA expression of Bax in the model group were significantly increased and the expression of Bcl-2 was significantly decreased (P<0.01). Hawthorn extract also reduced the protein and mRNA expression of Bax and increased the Bcl-2 expression in the aorta (P<0.01).@*CONCLUSION@#Hawthorn extract has anti-atherosclerosis and stabilizing unstable plaque effects. The mechanism may be related to the inflflammation and apoptosis signaling pathways.
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Animals , Male , Aorta , Pathology , Apoptosis , Atherosclerosis , Blood , Drug Therapy , Crataegus , Chemistry , Inflammation , Blood , Drug Therapy , Inflammation Mediators , Metabolism , Lipids , Blood , Mice, Inbred C57BL , Plant Extracts , Pharmacology , Therapeutic Uses , RNA, Messenger , Genetics , Metabolism , bcl-2-Associated X Protein , MetabolismABSTRACT
Endothelial to mesenchymal transition(EndMT) plays a major role during organism development, and also contributes to several adult cardiovascular diseases.EndMT-derived fibroblast-like cells are common in atherosclerotic lesions.Pro-atherosclerosis factors, such as oxidative stress, hypoxia, inflammatory cytokines and oscillatory fluid shear stress can promote EndMT.EndMT is closely associated with plaque calcification, and unstable and ruptured plaque phenotype that may prone to cause clinical events.EndMT may be another key step in the prevention and treatment of atherosclerosis.Here, we reviewed the role played by endothelial-to-mesenchymal transition(EndMT) and its key regulators in atherosclerosis.
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<p><b>OBJECTIVE</b>To observe the effects of red yeast rice (RYR) on blood lipid levels, aortic atherosclerosis (AS), and plaque stability in apolipoprotein E gene knockout (ApoE-/-) mice.</p><p><b>METHODS</b>Twenty-four ApoE-/- mice were fed with a high-fat diet starting from 6 weeks of age. Mice were randomized into three groups (n = 8 in each group): model group (ApoE-/- group), RYR group (ApoE-/- + RYR group), and simvastatin group (ApoE-/- + simvastatin group). Eight 6-week-old C57BL/6 mice were assigned as the control group and fed with a basic diet. After 36 weeks, plasma lipids and inflflammatory factors were measured. Aortic atherosclerotic lesions by microscope, scanning electron microscope and transmission electron microscope were observed. Plasma levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured with enzyme-linked immunosorbent assay. The level of high sensitivity C-reaction protein (Hs-CRP) was detected by the scattering immunoturbidimetric assay. Protein expression of matrix metalloproteinase-9 (MMP-9) and nuclear factor κB (NF-κB) in aorta were tested by immunohistochemistry.</p><p><b>RESULTS</b>Compared with the model group, treatment with RYR significantly decreased the levels of total cholesterol, triglyceride, low-density lipoprotein cholesterol, lipoprotein (a), and apolipoprotein B100 in ApoE-/- mice (P<0.01). Compared with the model group, treatment with RYR decreased the levels of Hs-CRP, IL-6, and TNF-α (P<0.01). RYR also reduced the protein levels of NF-κB and MMP-9 of the aorta.</p><p><b>CONCLUSIONS</b>RYR has the anti-atherosclerotic and stabilizing unstable plaque effects. The mechanism might be related to the inflflammatory signaling pathways.</p>
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Objective To study the relationship between serum salusin-α and lipoprotein associated phospholipase A2(Lp-PLA2) in carotid unstable plaque with cerebral infarction. Methods One hundred patients with carotid unstable plaque confirmed by carotid ultrasound, divided into two groups as follows:cerebral infarction group (CI group, n = 50) or without cerebral infarction (plaque group, n = 50). We took 50 health subjects in the same period as control. The levels of serum salusin-α, Lp-PLA2 were detected by ELISA. Results Serum salusin-αlevel was significantly lower in the CI group than in the control group (P<0.01), and was also significantly lower in the CI group than in the plaque group (P < 0.01); Serum Lp-PLA2 level was obviously higher in CI group than in control group (P<0.05), and was also significantly higher in CI group than in plaque group (P < 0.05); The correlation between serum salusin-α level(OR = 0.140, 95% CI: 0.054-0.368, P<0.01) and cerebral infarction was significant in patients with unstable plaque. Conclusions The decrease of serum salusin-α level is significantly in patients with unstable plaque; the increase of Lp-PLA2 is significantly in patients with unstable plaque. The serum salusin-αlevel is a possible risk factor for cerebral infarction.
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Objective To study the feasibility of noninvasive detection of unstable plaques with ~(18)F-Fluorodeoxyglu-cose (~(18)F-FDG) PET/CT imaging. Methods Atherosclerotic plaques were induced in male New Zealand white rabbits. Animals were injected with FDG labeled with ~(18)F, then examined with PET/CT. Aorta was explanted for photography with digital camera, and ~(18)F-FDG uptake analysis. Thirty unstable plaques and 30 stable plaques were choosed so as to compare the quantitativly ~(18)F-FDG uptake. The number of macrophages and smooth muscle cells was detected by immunohistochemical technique. Results Experimental group showed inconsistent uptake of ~(18)F-FDG in the abdominal aorta. The results were confirmed in the ex vivo digital photo of the explanted aorta. The target to non target ratio (T/NT) and macrophages of unstable plaques were higher than stable plaques (P<0.01) , but smooth muscle cells obviously reduced (P <0. 01). Correlation analysis showed that there was a positive correlation between T/NT and macrophage content (r=0. 815,P<0. 01), and a negative correlation between T/NT and SMC content(r=-0. 684,P <0. 01). Conclusion ~(18)F-FDG PET/CT can constitute an attractive imaging method for the noninvasive detection of experimental unstable plaques.
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Objective To study the feasibility of noninvasive detection of unstable plaques with 18F-Fluorodeoxyglucose (18F-FDG) PET/CT imaging. Methods Atherosclerotic plaques were induced in male New Zealand white rabbits. Animals were injected with FDG labeled with 18F,then examined with PET/CT. Aorta was explanted for photography with digital camera,and 18F-FDG uptake analysis. Thirty unstable plaques and 30 stable plaques were choosed so as to compare the quantitativly 18F-FDG uptake.The number of macrophages and smooth muscle cells was detected by immunohistochemical technique. Results Experimental group showed inconsistent uptake of 18F-FDG in the abdominal aorta. The results were confirmed in the ex vivo digital photo of the explanted aorta. The target to non target ratio(T/NT) and macrophages of unstable plaques were higher than stable plaques(P
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Objective:To investigate the effect ofLeech Capsule on stability ofcarotid plaque and expression ofplatelet membrane glycoprotein in patients with cerebral arteriosclerosis.Methods:203 patients with cerebral arteriosclerosis which with unstable carotid plaque were divided into two groups.There were 101 patients in observation group which were treated by conventional therapy and Leech Capsule, and 102 patients in control group which were treated only by conventional therapy.Then comparison analysis ofIMT, plaque area, unstable plaque number and positive rates ofPAC-1 and CD62P were made before and after treatment with two groups.Results:After treatment, the IMT, plaque area, unstable plaque number and positive rates ofPAC-1 and CD62P in observation group were significantly lesser than those in control group.In observation group, all parameters after treatment were significantly lesser than those before treatment, but in control group there were no significant difference in IMT and positive rates ofCD62P between after treatment and before treatment.In addition, there were no obvious adverse reactions after treatment by leech capsule.Conclusion:Leech Capsule was an effective drug for stabilizing carotid plaque and depressing the level ofplatelet activation, and it had few adverse reaction.It was worth further spreading.
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s: Recently, following the development of basic experimental research, great progress has been acquired in the fields of the understanding and management of the acute coronary syndromes (ACS). This review summarizes the molecular and cellular bases, the management of the unstable plaque, risk stratification and the management of ACS.
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Objective: To examine the effect of Benapril on atherogenesis and the plaque rupture in rabbits.Methods: Thirty four healthy male New Zealand white rabbits were randomly divided into 4 groups.Group C (control group) was fed normal diet for 10 weeks,group HL fed 1% cholesterol diet,group B fed 1% cholesterol diet and Benapril 5 mg/d.Ten rabbits of plaque rupture group were fed 1% cholesterol diet for 10 weeks with atherosclerosis induced by left carotid iliac damage.Ten weeks after the initiation of the diet,an angioplasty was performed.After angioplasty,the surviving rabbits( n =10) were randomized to receive benapril(5 mg/d,each) supplementation in drinking(B group, n =4) or no treatment(untreated group, n =4). The levels of CEC were measured by morphometrical counts at different periods(the 5th week,the 10th week).Before and 5,10 weeks after experiment,fasting blood samples were collected for serum total cholesterol(TC),high density lipoprotein cholesterol(HDL C),low density lipoprotein cholesterol(LDL C),and triglyceride(TG) assay.The levels of plasma circulating endothelial cells(CEC) were measured by morphometrical counts and the levels of plasma von Willebrand factor(vWF) were determined by ELISA.After sacrificing the separated, entire aortas were stained with oil red O and then processed for histological examination;planimetry was done with a computer system.Endothelial cells were confined by the presence of Factor Ⅷ related antigen as the specific cell marker.Results: The serum TC,TG,LDL C increased progressively in group B and group HL,but the levels of vWF in group HL were significantly higher than that in group B on the 5th and 10th respetively( P