Study on the association between helicobacter pylori infection and atherosclerosis
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Objective:( 1) To observe the corraltion between Helicobacter pylori and Cerebral atherosclerosis( stanosis).( 2) To establish a stable model of Helicobacter pylori infection and atherosclerosis. Methods:( 1) Fourty-two New Zealand rabbits were randomized into a control group and an experimental group; control group was given an standard diet,experimental group was fed with high-fat diet. Six weeks later blood lipids was detected,rabbit model of hyperlipidemia was established.( 2) At the same time,according to different processing factors,the experimental group were randomly divided into high fat diet group、Hp infected group and anti-Hp group. Hp infected group and anti-Hp group were injected with standard Hp strain. Anti-Hp group received anti-Hp treatment,and Serum lipid levels,Hcy,hs-CRP,IL-6 were determined during the 6th,8th and 12 nd week of experiment,and CDUS was used to detect the rabbits' s carotid artery intimamedia thickness,plaque size. Results:( 1) To establish Hyperlipidemia model in rabbits,blood Lipid levels at each time point had no obvious change in the high fat diet group,which meant hyperlipidemia was in steady state.( 2) Establish the hyperlipidemia model in rabbits. No significant changes of high fat diet groups in the blood lipid levels of hyperlipidemia,forming stable. Compared with the 6th week experiment,the levels of TC、TG、LDL-C、Hcy、hs-CRP、IL-6 were significantly increased and HDL-C was decreased in Hp infected group during the 8th、12t week( P 0. 05). Anti-Hp group at different time points of the experiment,blood biochemical indexes did not change obviously( P 0. 05).( 3) Three groups of IMT of carotid artery were thickened during the 8th week,Hp infection group formed a small plaque,and the other groups without plaque formation; three groups were formed plaque during the 12 th week( P 0. 05). Conclusion: In Hyperlipidemia model of rabbit,Hp infection could promote chronic inflammation and elevated serum lipid. Hp infection may aggravate the degree of atherosclerotic lesions,It is suggested that Hp infection may affect the inflammatory reaction and lipid metabolism to promote progression of atherosclerosis,At the same time,the anti Hp therapy can reduce inflammatory reaction and blood fat,reduce the severity of carotid atherosclerosis.Keywords:
Hyperlipidemia
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Objective To establishe chronic periodontitis (CP) model in rats, and to explore the effects of various periodontal interventionson the development of artery atherosclerosis (As) in SD rats. Methods 42 male SD rats were fed regular chow for 2 weeks ,and were randomly divided into three major groups: Group A (normal control), Group B (As) and Group C (CP). SD rats in Group C were simulated all kinds of periodontal interventions and further divided into Group C1 (no treatment), Group C2 (scaling and root planning), Group C3 (systemic antibiotics) and Group C4 (tooth extraction). For each group, the SD rats were processed for pathology evaluation at 24 weeks after the establishment of the corresponding model. The pathological lesion of carotid artery plaque was stained with hematoxylin and eosin. Five times serum hs-CRP levels were evaluated before and after periodontal interventions by ELISA. Lipid plaque formation of Group A, B and C1 was assessed under light microscope using oil red staining. Results Oil red under light microscope observation in the carotid artery of Group A were not accumulation of lipid deposits. However, accumulation of lipid deposits was observed in Group B(atherosclerosis) and Group C1. Histologic sections showed that increased foam cells infiltration and inflammatory cells in Group B (atherosclerosis), Group C1 (not any intervention) and Group C3 (systemic antibiotics) were evident, Smooth muscles cells had undergone the heaviest degeneration in the artery media, and elastic fibers were also disordered in the artery media. In Group C2 (scaling and root planning) inflammatory cells were not found, and there was only a small amount of vacuolar changes. Obvious thickening of the vessel wall, the intimal inflammatory cell adhesion , and the formation of foam cells in the artery media were observed in Group C4. The serological testing hs-CRP discovered CRP levels of Groups A, B, and C1 were increased with the passage of time. CRP levels of Groups C2, C3, C4 reached a peak over time one week after the second intervention , and were significantly higher than Group B and Group C1. The difference was statistically significant (P 0.05), then gradually declined. Group C2 was significatly reduced and lower than Groups B and C1 (P 0.001 ). Conclusions In chronic periodontitis of rats, permanent periodontitis can cause the risk of atherosclerosis. No effective improvement could be observed on the As lesions with the systemic antibiotics treatment . Initial periodontal therapy (scaling and root planning) may reduce the risk of atherosclerosis. Tooth extraction may also have a long-term and effective intervention measures.
Group B
Group A
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Objective To observe effect of Bererine on regressing atherosclerotic plaques,and to investigate its possible mechanisms.Methods Forty New Zealand White Rabbits were randomly divided into four groups( 10 /group). Blood samples were collected in different periods to measure lipid profile and to quantify the plasma concentration of different inflammation mediators. The aorta was dissected and excised to observe the occurrence of plaque rupture and thrombosis. The abdominal aorta was processed and examined by hematoxylin and eosin staining. Histopathological slides were analyzed by use of a computer-assisted morphometric analysis system,the intima and Tunica media vasorum thickness were measured. Results Nine rabbits in group 1,2 and group 3,and 8 rabbits in group 4 completed the study. Plaque rupture and thrombosis occurred in five rabbits from the remaining nine rabbits in group 2 after pharmacological triggering,while there were no plaque rupture in the other three groups. Serum TC,TG,LDL-c and inflammation mediators levels of Berberine group and simvastatin group was decreased compared with high-cholesterol group( P 0. 05),and they were both much higher than those of normal diet group. In contrast,no significant differences were found between Berberine group and simvastatin group. Pathologic staining demonstrated that the intima was thin and complete in group 1. A great quantity of widespread fatty plaque were seen in group 2,in which intima thickened and foam cell accumulated obviously. In contrast,in the berberne prevention group and the simvastatin control group,plaque thickness diminished and both quantity and volume of foam cell decreased. The intima and Tunica media vasorum thickness in group 2 were significantly higher than the corresponding values in the berberne prevention group or the simvastatin control group. The I /M of artery in the group 2 was higher than that in the berberine prevention group or simvastatin control group( P 0. 01). There was no significant difference between the berberine prevention group and the simvastatin control group( P 0. 05). Conclusion Berberine had the effect on preventing the formation of the artery atherosclerosis and stabiling vulnerable plaques. Lipid and anti-inflammation mechanisms contribute to the beneficial effects of BBR in artery atherosclerosis formation and in plaque stability.
Vasa vasorum
Tunica media
Foam cell
Abdominal aorta
Tunica intima
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AIM:To explore the expressive role of lipoprotein-associated phospholipase A2,high sensitive C-reactive protein and matrix metalloproteinase-9 in vulnerable atherosclerotic plaques in a rabbit model. METHODS: Forty eight New Zealand white male rabbits were randomly divided into 4 groups (12 rabbits each): control group,stable plaque group,p53 group,and p53+drug group. Rabbits in control group were fed with a regular diet and underwent sham operation. Rabbits in stable plaque group,p53 group and p53+drug group underwent balloon induced arterial wall injury and then were fed on a diet with 1% cholesterol. The animals were all fed for 3 months,then the rabbits in p53 group and p53+drug group underwent Ad5-CMV p53 transfection at 10th week. Before killed,the animals in p53+drug group underwent pharmacological triggering with Russell's viper venom (RVV) and histamine to induce the rupture of the atherosclerotic plaques. At the 1st day and before sacrifice,the serum was collected for measuring Lp-PLA2,hs-CRP,MMP-9,HDL,LDL and VLDL. The expressions of Lp-PLA2,hs-CRP and MMP-9 in tissues were determined by the methods of hybridization and immunohistochemistry. RESULTS: At the end of 12th week,the serum and tissue levels of Lp-PLA2 and MMP-9 in stable plaque group,p53 group and p53+drug group were significant different from those in control group and in each group at the first day (P0.05). The serum levels of Lp-PLA2 and hs-CRP in p53 group and p53+drug group were significantly higher than those in control group and stable group (P0.05). The serum levels of Lp-PLA2,hs-CRP and MMP-9 were all significantly different between p53 group and p53+drug group (P0.05). At the end of 12th week,pathological results showed that 4 groups were normal artery,stable plaque,vulnerable plaque and rupture plaque,respectively. The fabric cap was thicker in plaque groups than that in normal group (P0.05). The rupture and formation of thrombus were more significant in p53+drug group than those in p53 group. The serum level of Lp-PLA2 had negative interrelated relationship with fabric cap in plaque groups (r=-0.710,P0.01),and hs-CRP,MMP-9 had no interrelated relationships with fabric cap in plaque groups. CONCLUSION: Base on the successful establishment of the atherosclerotic plaque animal model,serum Lp-PLA2 shows better interrelated relationships to plaques stability. Combination with hs-CRP and MMP-9,we can exactly evaluate the nature of plaques.
Group A
Vulnerable plaque
Group B
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Aim To evaluate liver histological lesions of atherosclerosis animal models induced by high lipid diet in New Zealand White rabbits. Methods Normal male New Zealand White rabbits (n=14) were randomly divided into two groups: control group (n=6) and atherosclerosis group (n=8). Atherosclerosis was induced by high lipid diet (92% normal rabbit chow with 2% cholesterol and 6% lard). Rabbits were sacrificed at the end of week 10. Serum aminotransferase, lipid levels and fasting plasma glucose (FPG) levels were examined dynamically and morphology changes in ascending aortas and livers were observed. The intima-to-media (I/M) ratio of ascending aortas was also measured. Results The levels of serum aminotransferase, lipid and FPG levels in atherosclerosis group were significantly higher than those of control group (P0.05). Compared with control group, the livers presented the pathology of hepatic steatosis and steatohepatitis in atherosclerosis group, and ascending aortas showed typical atherosclerosis changes. The mean I/M ratio in ascending aortas of atherosclerosis group (1.13±0.32) was higher than control group (0.12±0.04, P0.05). Conclusion High lipid diet can induce an ideal rabbit model of atherosclerosis, and also induce severity liver histological lesion, and may be a right method to create the rabbit model in researching the relationship between fatty liver and atherosclerosis.
Steatosis
Steatohepatitis
Lipid Profile
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Objective To study the effect of clopidogrel on the endothelial function of the rabbit with experimental atherosclerosis(AS). Methods Twenty-seven New Zealand male white rabbits were randomly divided into 3 equal groups: ① normal control group,②model control group and ③ drug treatment group.Rabbits of group ① were fed on a diet(100 g·d-1) containing no cholesterol for 12 consecutive weeks.Rabbits of group ② and group ③ were fed on a diet(100 g·d-1)containing 1.5% cholesterol for 12 consecutive weeks as well.In the meantime,rabbits of group ③ were given each 4 mg·kg-1 of clopidogrel administered by gastrogavage q.d..At the end of the 12th week,blood samples were collected from the central artery of the ear.Serum lipids were determined with enzymic methods,serum endothelin(ET) and hypersensitive C responsive protein(hs-CRP) were assayed with ELISA and serum nitric oxide(NO) was determined with the oxidase method.Specimens of the aortic arch were taken and morphometry was used to calculate the ratio of the area of the atherosclerotic plaques to that of the intima and the ratio of the thickness of the intima where the plaque was most prominent to that of the media. Results Serum lipid,ET,and hs-CRP levels in animals of group②(the model control group) and group ③(model + clopidogrel treatment) were obviously higher than those in animals of group ①(normal control)(P0.05).In contrast,serum NO levels in rabbits of group ② and group ③ were significantly lower than those in rabbits of group ①(P0.05).The difference between animals of group ② and group ③ with respect to the serum lipid levels was not significant.However,serum ET and hs-CRP levels in animals of the model control group were significantly higher while serum NO contents were strikingly lower than those in rabbits treated with clopidogrel(P0.05).Morphologically,the atherosclerotic lesions in the aorta were of much less severity in rabbits of the drug treated group(group ③) than those of the model control group. Conclusion Clopidogrel was shown to inhibit the formation of atherosclerotic plaques and protect the function of the vascular endothelium,and these effects of the drug may be related to its inhibitorty action on the local inflammation of the artery.
Lagomorpha
Animal model
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Objective To study the role of serum TNF-α level in formation of atherosclerotic plaques. Methods Ten male big ear rabbits were randomly divided into model group(group A, n=5) and normal control group(group B, n=5). After damage to abdominal aorta intima was induced with balloon, the animals in group A were fed with high fat diet for 15 weeks while those in group B were fed with normal diet for 15 weeks. Fasting blood was taken from the ear marginal vein to measure the serum levels of TC, TG, HDL-C, LDL-C and TNF-α before and by the end of week 15. The animals were killed. Their abdominal aorta was isolated and observed under optical microscope. Apoptosis was detected by TUNEL. Results The animal atherosclerosis model was successfully established. The serum levels of TC, TG, LDL-C and TNF-α were significantly higher in group B than in group A(P 0.05). The serum levels of TC, TG and LDL-C were positively related with the serum TNF-α level(P 0.05). However, the serum HDL-C level was not significantly related with the serum TNF-α. level. The serum TNF-α level was positively related with the apoptosis index in abdominal aorta plaques. Conclusion TNF-α may be involved in apoptosis in atherosclerotic plaques. Serum levels of TG, TC, LDL-C and TNF-α are the risk factor for atherosclerosis.
Abdominal aorta
Normal group
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Objective To observe the influence of rosuvastatin on IL-8 and its expression in rabbit atherosclerosis model.Methods 30 New Zealand rabbits were randomly divided into three groups: control group(n=10),experiment group(n=10) and treatment group(n=10).Animals in control group received normal diet,the other two groups received arterial intimal injury of carotid with balloon after four weeks experiment feeding,then treated with experiment,experiment and rosuvastatin for six weeks,respectively.3 ml blood was drawn from the ear vein of all the rabbits after the carotid arterial intimal injury(at the end of the fourth week) and before sacrifice(at the end of the tenth week).Lipid and IL-8 levels were measured.At the end of the experiment,all rabbits were sacrificed,the carotid arteries were isolated and paraffin-embedded slices and immunohistochermical staining of IL-8 were performed.Results Compared with control group,Lipid and IL-8 levels in treatment group and experiment group were significantly increased at the end of 4 weeks(P0.05),and lipid and IL-8 levels in treatment group were significantly lower than experiment group at the end of 10 weeks(P0.05);There were no arteriosclerosis lesions and IL-8 expression in the carotid arteries of control group;compared with experiment group,intima area(IA),ratio of intima area to membrane area(I/M),luminal stenosis degrees(LSD) and the expression of IL-8 on atherosclerotic plaque were significantly decreased in treatment group(P0.05).Conclusion Rosuvastatin can reduce IL-8 level and decrease expression of IL-8 in atherosclerosis plaques.It demonstrates that rosuvastatin may inhibit the progression of atherosclerosis by reducing the inflammatory action.
Arteriosclerosis
Tunica intima
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Objective To establish a rat atherosclerosis(AS) model by immune injury and high-fat feeding.Methods The rat model was established by the following procedure: Wistar rats(body weight 130-150 g) aged 5 weeks were included in this study.The rats received intraperitoneal injection of ovalbumin(OVA) and i.v.injection of bovine serum albumin,and were fed with high-fat feed plus vitamine D_3 and drinking water added with ferrous sulfate(FeSO_4).The serum lipid level and blood biochemical indexes were monitered and pathological changes were examined.Results The TC,HDL,LDL values in the AS models were 6.1±2.52,2.46±1.01,3.76±1.67 and 1.3±0.10,1.02±0.13,0.52±0.063,respectively,(P0.05),statistically significantly higher than those of normal control animals.The value of C-reactive protein,CK and CK-MBb in the high fat feeding group was statistically significantly higher than those of normal control animals(4.99±2.26,996.3±82.8,669.5±82.8;0.183±0.160,293.8±167.1;177.5±86.5;P0.05).The animals fed with high fat diet and treated by immune injury were identified by HE staining.As a result,plaques appeared in their aorta.Conclusions The method utilized in this study can induce the production of hyperlipemia and led to local myocardial ischemia,then to the damage of myocardium and occurrence of myocardial inflammation.It renderes the constitutes of plaques deposited in vascular wall,and finally leading to arterial plaques formation.In summary,a model of atherosclerosis plaque model can be established in a shorter period of time by this method.
Intraperitoneal injection
Atheroma
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Objective:To study the effect of Chinese medicine “Qishenjiangzhi decoction”(QSJZD) on atherosclerosis (AS) and to elucidate its mechanism further. Method:Twenty-four healthy male SD rats were randomly divided into 3 groups:control group, model group ,Chinese medicine treated group, The model rats of atherosclerosis were established by feeding with high cholesterol diet and injecting with vitamin D_2 for 6 weeks. Six weeks later, serum lipid levels of MDA, SOD and lipid were measured for all the rats. HE staining was used to study the pathology change of atherosclerosis. Immunohistochemistry and gelatin zymography were used to detect the expression and activity of MMP-2 in aorta vessel. Result:Comparing the chinese medicine treated group with model group, the serum level of TC, LDL-C and MDA were significantly reduced (P0.01) , while serum SOD level was obviously increased (P0.01) .The damage of the aortas in medicine treated group was less severe than that in model group. The expression and activity level of MMP-2 in medicine treated groups was significantly higher than the model groups. (P0.01). Conclusion:QSJZD could intervene the formation of atherosclerosis, The mechanism might be through suppressing TC, LDL-C and lipid peroxidation, and affecting the activity and expression of MMP - 2.
Decoction
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Objective: To evaluate the connection of plaque angiogenesis and progression of atherosclerotic plaque. Method:Fifteen rabbits were randomly divided into three groups , control group ( n =5) fed with common diet and other groups(high cholesterol group, n =5; VEGF group, n =5) fed with high cholesterol diet. Albumin or VEGF165 was administered by a single-intramuscular injection (2 μg/kg) to rabbits fed with cholesterol diet or common diet at beginning 3 weeks before therapy. Subsets of rabbits from each group were underwent perfusion fixation and harvesting of the thoracic aorta for morphometric and immunohistochemical analysis at 42 days. Moreover, the changes of serum level of IL -8 and TC in the corresponding time points and groups were determined as well. Result:①Significant difference was shown in comparing mean plaque area[(control-group 0% , high-choles-terol-groupd. 81 ±0. 61)% , VEGF-group (24. 12±3. 58)%)], plaque circumference [Control-group 0,high-cholesterol-group (6. 05±1. 62)% , VEGF-group (25. 71±2. 97)%] and maximal plaque thickness (control-group 0, high-cholesterol-group (0. 06±0. 002)mm, VEGF-group (0. 16 ± 0. 007) mm] respectively.②There were significant differences in neovascularization density [number of CD34-positive cells (cells/mm2) control group 0, high cholesterol group (12. 35±2. 02) % , VEGF-group(61. 15±7. 55)% , P 0. 05)] in control- group, high cholesterol groups and VEGF group at 42 day. ③TEM(transmission electron microscopy )image was shown intimal vessels associated with lesion and the capillary lumen contain lymphocytes.④There was positive correlation of Neovascularization (CD34 positive area )with plaque area( r =0. 989, P 0. 01)in VEGF-group at 42 day.⑤ Significant difference was shown in comparing levels of serum IL-8 in the corresponding time points and groups, but there is no significant difference in comparing levels of serum TC in the corresponding time points and groups. Conclusion: Plaque angiogenesis potentially contributes to plaque development, and may correlate with inflammation.
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