YANG Chun-Tao , CAI Dian-Qi , BAI Hong-Bo , LIU Guo-Hui , LIU Xiao-Ai , XU Ji-De , and LI Yun-Quan
2013, 21(04):289-293.
Abstract:Aim To investigate whether reactive oxygen species (ROS) were involved in cobalt chloride (CoCl2) induced cellular proliferation in human pulmonary artery smooth muscle cells (HPASMC). Methods HPASMC were exposed to a chemical hypoxia agent CoCl2 to establish a cellular model of pulmonary arterial hypertension. An exogenous ROS donor, hydrogen peroxide (H2O2), was administered to examine the direct effect of ROS on HPASMC proliferation. Before the exposure of HPASMC to CoCl2 or H2O2, a ROS scavenger, N-acetylcysteine (NAC), was used to assess the effect of inhibitory oxidative stress on the cellular proliferation induced by the two agents above. Cell proliferation was measured by cell counter kit 8, expression of hypoxia inducible factor-1α (HIF-1α) was tested by Western blot assay and intercellular ROS were observed by 2′,7′-dichlorfluorescein-diacetate staining followed by photofluorography. Results Treatment of HPASMC with CoCl2 for 24 h at concentrations ranging from 25 to 50 μmol/L induced significant cellular proliferation, and treatment with 50 μmol/L CoCl2 for 24 h obviously increased intercellular HIF-1α level. Similarly, treatment with H2O2 for 24 h at concentrations ranging from 12 to 25 μmol/L triggered cellular proliferation, however, treatment with H2O2 didn’t alter HIF-1α level in HPASMC. Pretreatment with NAC, prior to the treatment with CoCl2 or H2O2, statistically attenuated H2O2-induced HPASMC proliferation (P<0.05), but not CoCl2-induced cellular proliferation (P>0.05). Exposure of HPASMC to 50 μmol/L CoCl2 for 6-24 h didn’t alter intracellular ROS content. Conclusion ROS may not be involved in CoCl2-induced cellular proliferation in HPASMC.
WANG Gang , BIAN Yun-Fei , BAI Rui , ZHANG Na-Na , and XIAO Chuan-Shi
2013, 21(04):294-298.
Abstract:Aim To explore the impact of renin through angiotesin Ⅱ-independent mechanisms on calcification of rat vascular smooth muscle cells in vitro, and its molecular mechanisms.Methods Primary cultured cells were obtained by tissue-piece inoculation. Calcification of cultured rat vascular smooth muscle cells was produced by incubation with β-glycerophosphate and sodium pyruvate. The vascular smooth muscle cells were divided into 6 groups: the blank control group (cultured in normal medium), the calcification group (incubated in calcified medium), the calcification+angiotesinⅡ receptor blocker group (cultured in calcified medium, giving Losartan 10-6 mol/L to block AT1 and PD123,319 10-5 mol/L to block AT2), calcification+renin group (incubated in calcified medium, giving Losartan 10-6 mol/L and 10-5 mol/L PD123, 319, then added 10-10, 10-9, and 10-8 mmol/L renin). Calcification was confirmed by Von Kossa staining. Calcium content and alkaline phosphatase (ALP) activity were measured to estimate the extent of calcification. The mRNA expression of core binding factorα1 (Cbfα1) and transforming growth factor-β1 (TGF-β1) was measured by competitive quantitative RT-PCR. The expression of Cbfα1 protein content was measured by Western blot. Results Compared with the blank control group, the calcium content and ALP activity of the calcification group in creased significantly, as well as the mRNA expression of Cbfα1, TGF-β1 and the expression of Cbfα1 protein increased significantly (P<0.01). Compared with calcification group, calcification+ angiotensin Ⅱ receptor blocker group had no difference on calcification of vascular smooth muscle cells. Compared with calcification+angiotensin Ⅱ receptor blocker group, intervention of rennin (10-10, 10-9, 10-8 mmol/L) in a dose-dependent manner further promoted the calcium content and the ALP activity of rat vascular smooth muscle cells, as well as the mRNA expression of Cbfα1, TGF-β1 and Cbfα1 protein expression (P<0.05).Conclusions Renin can promote β-glycerophosphate-induced calcification of vascular smooth muscle cells through angiotesin Ⅱ-independent mechanisms, the mechanisms of renin promoted calcification of vascular smooth muscle cells through angiotesin Ⅱ-independent way may be through promoting the expression of TGF-β1, Cbfα1.
LI Qing , WANG Yi , ZHOU Qing , and WANG Yuan
2013, 21(04):299-304.
Abstract:Aim To establish early experimental atherosclerosis (As) rat model, and to investigate peripheral CD4+CD25+ regulatory T cells (Treg)/T helper 17 cells (Th17) imbalance and the effects of all-trans-retinoic acid (ATRA) on the balance in the model.Methods Fifty 8-week-old Sprague Dawley rats were randomly divided into 5 groups: the normal group, cholesterol diet group, immune injury group, cholesterol diet plus immune injury group, and cholesterol diet + immune injury + ATRA group (ATRA group). Rats in normal group and immune injury group were fed with normal diet, and other groups were fed with cholesterol diet. Rats in immune injury group, cholesterol diet plus immune injury group and ATRA group were immunized by ovalbumin. Rats in ATRA group were treated with ATRA. For all the 5 groups, the samples of blood and aorta were obtained after 16 weeks. The levels of serum lipids and cytokines were measured by ELISA Histological changes in aorta were analyzed by HE staining, and the frequencies of Th17 and Treg cells were detected by flow cytometry.Results A rat model of early As was established successfully. The results of HE staining showed that there was an edematous thickening in the intima and a mild atrophy in the membrane of cholesterol diet plus immune injury group, and there was also a less extent on pathological changes in immune injury group and ATRA group. Serum total cholesterol (TC) and low density lipoprotein cholesterol (LDLC) concentrations in cholesterol diet group and cholesterol diet plus immune injury group were markedly increased compared with those in normal group and immune injury group (all P<0.05), but the levels of serum lipids in ATRA group had no significant difference compared with those in other groups. Expression of Treg and relative cytokines (interleukin-10 (IL-10), transforming growth factor beta (TGF-β)) was significantly lower while expression of Th17 and relative cytokines(IL-17, IL-6) was obviously higher in immune injury group and cholesterol diet plus immune injury group than those in normal group and cholesterol diet group (all P<0.05). The levels of Treg and relative cytokines were significantly increased while the levels of Th17 and relative cytokines in ATRA group were markedly decreased than those in cholesterol diet plus immune injury group (all P<0.05).Conclusions An early As rat model was successfully established by immune injury and cholesterol diet. The shift of the Th17/Treg balance from Treg cells towards Th17 cells exists in rat model, and ATRA may play an important role in inhibiting As development by influencing the peripheral Th17/Treg balance.
ZHONG Ying-Jie,ZHANG Zi-Wei,XU Yu,HUA Xiao-Min,and HU Yun
2013, 21(04):305-310.
Abstract:Aim To assess the effect of atorvastatin on ApoE-/- mice atherosclerosis and calcification. Methods Six week old male ApoE-/-mice were fed with diets containing 45% kcal from fat . The mice received diets ad lib for 8 weeks and had free access to water. Then the mice were randomly divided into two groups: atorvastatin group(n6) or high fat group (n6). After 8 weeks of diet, mice were killed,blood was collected and plasma TG,TC,HDL-C,LDL-C,IL-6 and A-SAA concentrations were measured. Aotic sections were stained with hematoxylin and eosin or von kossa and observed under microscope. Immunohistochemical staining was performed to visualize the expresssions of vascular MCP-1,VCAM-1and BMP-2. Human Aorta Endothelial Cells(HAEC) were treated with different doses of atorvastatin. The level of BMP-2,calcium content and AKP activity were measured. Results Serum levels of TG,TC,LDLC,IL-6 and A-SAA in the atorvastatin group significantly decreasd compared with those in the high fat group(P<0.05). Atherosclerotic plaques were observed in ApoE-/- mice of the high fat group. And the plaque lesions revealed more limited in atorvastatin groups compared with those in the high fat group. However,the calcium mineral deposits on vascular tissue induced by atorvastatin were stronger than the high fat group(P<0.05). The expressions of vascular MCP-1 and VCAM-1 in atorvastatin group significantly decreased compared with those in the high fat group(P<0.01). However,the expression of BMP-2 in atorvastatin group was increased compared with the high fat group(P<0.01). Atorvastatin increased HAECs BMP-2 expression compared with the control group(P<0.05),and further increased the calcium deposition and the activity of AKP significantly compared with the control and low-dose atorvastatin group (P<0.01,P<0.05). Conclusion Atorvastatin may reduce the levels of serum TG,TC,LDLC,IL-6 and A-SAA,decrease the expressions of vascular MCP-1,VCAM-1 and inhibit the progression of atherosclerosis lesion in ApoE-/- mice. However, Atorvastatin may increase the expression of BMP-2 and accelerate calcium deposition, stimulate the HAEC calcification and the activity of AKP, thus affect calcification of aortic tunica intima.
XU Xuan-Xuan , YIN Kai , LI Tao , LI Jin-Feng , TU Jian , WANG Zuo , and TU Yu-Lin
2013, 21(04):311-314.
Abstract:Aim To observe the effect of Cyclophilin A on the expression of nuclear factor-κB (NF-κB) protein in RAW264.7 cells induced by oxidized low density lipoprotein (ox-LDL). Methods Western blot was applied to detect the expression of Cyclophilin A and NF-κB protein in RAW264.7 cells induced by ox-LDL. Western blot was applied to detect the expression of Cyclophilin A and NF-κB protein in Cyclophilin A siRNA RAW264.7 cells induced by ox-LDL. Results The expression of Cyclophilin A and NF-κB protein in RAW264.7 cells was up-regulated by ox-LDL. Cyclophilin A siRNA could down-regulate the expression of NF-κB protein. Conclusion The change of the CypA protein expression could down-regulate the protein expression of NF-κB in RAW264.7 cells induced by ox-LDL.
GAO Ting , LU Yu-Sa , DONG Ze-Bo , GONG Fei-Yu , and QU Run-Bo
2013, 21(04):315-319.
Abstract:Aim To explore the influence of high-cholesterol to islet beta cell and intervention effect of atorvastatin. Methods Twenty-four New Zealand white rabbits were randomly divided into control group, cholesterol group and atorvastatin group, with eight rabbits in each group. After feeding for six weeks, the empty stomach blood were collected for inspected fasting blood- glucose (FBG), insulin (FINS), total cholesterol (TC), low density lipoprotein cholesterol (LDLC) and triglyceride(TG) The oral glucose tolerance test (OGTT) were examined The pancreatic tissue was taken to observe islet morphology and insulin positive cells by immunohistochemical method,to detect proinsulin mRNA expression by RT-PCR, to measure oxidative stress index: malondialdehyde (MDA) and reducing glutathione (GSH) by spectrophotometry. Results In cholesterol group after sugar load of 30 and 60 min, the blood glucose, the date of aera-under-curve(AUC) and the insulin resistance index (HOMA-IR) was increased (P<0.05), and insulin sensitive index (ISI), beta cell function index (HBCI/IR) was lower than control group (P<0.05) A great deal of beta cell hypertrophy and arrangement disorder were observed in the cholesterol group,in addition,insulin positive expression was increased The proinsulin mRNA was over-active(P<0.05) MDA absorbance value was higher than that of the control group (P<0.05), and GSH absorbance value was just the opposite (P<0.05). In atorvastatin group insulin positive expression decreased compared with high cholesterol group, MDA absorbance value was lower (P<0.05), and GSH absorbance value was just the reverse (P<0.05). Then, fasting gloucose, blood glucose after sugar load of 120 min, HOMA-IR, HBCI/IR, ISI and proinsulin mRNA express had no significant difference. Conclusions Hypercholesterolemia may induce pancreas oxidation-antioxidation system imbalance, finally lead to islet beta cell morphology and function damage. Atorvastatin can significantly reduce pancreatic tissue oxidative stress, but can not improve the sugar metabolic disorders induced by high cholesterol.
XIE Yuan-Xing , WANG Hong-Yun , WANG Zhi-Yun , SHEN Hong-Ming , LIU Ying , and XI Zhen-Chuang
2013, 21(04):320-324.
Abstract:Aim Using multiple tracking techniques (MTT) to analyze and evaluate the changes of atherosclerosis plaque biomechanics patients with metabolic syndrome (MS). Methods 126 patients with metabolic syndrome according to the diagnostic standard of International Diabetes Federation (IDF) and 60 normal subjects were examined using multiple tracking techniques, which dynamic imaging was acquired from all subjects and all above images were stored for off-line analysis with dedicated MTT workstation and all mechanical parameters were collected, including the peak velocity, strain and strain rate of plaque and without plaque, the cap and shoulder of plaque, intima media thickness. The above parameters at different points of carotid intima were compared and studied. Results The level of intimal-media thickness (IMT) in MS patients was higher than that in normal control contract (P<0.05). The systolic maximum velocity and strain of carotid with normal control were significantly higher than that of carotid without plaque with MS (P<0.05). The systolic maximum velocity and strain rate of soft plaque were increased significantly than those of hard plaques. The systolic maximum velocity and strain rate of fabric cowl in the plaque were significantly lower than the shoulder of the plaques (P<0.05). Conclusion The MTT could detect the elasticity of blood vessel wall, sclerosis and the mechanism asynchrony of the carotid artery, and then could be used as the predictive parameter and quantization for atherosclerosis and vulnerable plaque instability.
DU Li-Li , LV Ze-Ping , LIU Cheng-Wu , LUO Huan , HU Cai-You , YANG Ming , SONG Zhen , PENG Jun-Hua , LUO Xiao-Qiu , ZHOU Xiao-Ling , YIN Rui-Xing , and PAN Shang-Ling
2013, 21(04):325-330.
Abstract:Aim To investigate the plausible relationship between the polymorphism of methylenetetrahydrofolate reductase (MTHFR) gene at C677T locus and serum lipid levels and longevity in the long-lived cohort residing in Guangxi Hongshuihe River Basin. Methods Genotyping was performed with PCR-RFLP technique for 505 long-lived Zhuang individuals inhabiting in Guangxi Hongshuihe River Basin whose ages were 90 and above (long-lived group, LG) and 468 ethnic- and geographic-matched healthy mid-aged or elderly controls (non-long-lived group, non-LG). Association analysis were undertaken between MTHFR C677T genotypes and serum lipids (total cholesterol, TC triglyceride, TG high density lipoprotein, HDL low density lipoprotein, LDL). Results The allelic (C and T) and genotypic (CC, CT, and TT) frequencies of the LG and non-LG were 80.2%, 19.8% versus 85.0%, 15.0% and 65.5%, 29.3%, 5.2% versus 73.9%, 22.2%, 3.8%, respectively, which displayed significant differences between the two tested groups, with an overrepresentation of T allele in long-lived females specially, but not in males. On lipid profiles, the levels of TC, TG, LDL in LG are significantly higher than that in the non-LG. After stratifying by MTHFR C677T genotype and gender, the TC, TG, and LDL levels were noted dramatically higher in females but not in males harboring the mutant genotype (CT/TT) than that of the non-T carriers (CC) in the LG. Conclusions Our data suggest that there was a femalespecific association between the MTHFR C677T polymorphism and serum lipid levels and human longevity, which may be one of the molecular genetic basis for the longevity in the Guangxi Hongshuihe River Basin.
SU Ke,LONG Yan , HUANG Li-Li , XUN Jun-Qiong , SI Lian-Dong , PENG Ying , and HU Jing
2013, 21(04):331-335.
Abstract:Aim To explore the relationship between atherosclerosis and serum interleukin-10 (IL-10), adiponectin in type 2 diabetes patients with hyperuricemia. Methods The blood uric acid (UA), serum interleukin-10 (IL-10), adiponectin and other indicators were detected in type 2 diabetes patients with high uric acid and artery atherosclerosis sclerosis (65 cases, high uric acid group), type 2 diabetes patients with artery atherosclerosis sclerosis (68 cases, normal uric acid group), normal control group (30 cases), respectively. And the relationship between the above indexes and artery atherosclerosis were analysed. Results Serum IL-10 levels was significantly lower in high uric acid group, normal uric acid group than that in normal control group, and it was lower in high uric acid group than that in normal uric acid group Serum adiponectin levels was significantly lower in high uric acid group, normal uric acid group than that in normal control group, and it was lower in high uric acid group than that in normal uric acid group Correlation analysis showed that intima-media thickness (IMT) was negatively correlated with IL-10 and adiponectin, and positively correlated with homeostasis model assessment insulin resistance index (HOMA-IR), UA. Multiple linear stepwise regression analysis showed that IL-10, adiponectin, UA, triglyceride (TG), low density lipoprotein cholesterol (LDLC), HOMA-IR, systolic blood pressure (SBP) and dglycosylated hemoglobin (HbA1c) entered the regression equation. Conclusion Reduction of serum IL-10, adiponectin levels is closely related to insulin resistance, hyperuricemia, which participate in the development of diabetic atherosclerosis.
WANG Xiao-Qi , DU Nai-Li , ZHANG Lei , and LI Zhen-Hua
2013, 21(04):336-340.
Abstract:Aim To investigate the alteration and clinical significance of T-helper17 cells (Th17), interleukin (IL)-17 and IL-22 in patients with acute coronary syndrome (ACS). Method 50 patients were divided into three groups: acute myocardial infarction (AMI, n20), unstable angina (UA, n15), stable angina (SA, n15) 15 healthy subjects from physical examination were used as normal control group. The peripheral blood of Th17 and Th17/Th1 cells accounted for the proportion of CD4+T cells were detected by flow cytometry (FCM) the concentration of plasma IL-17 and IL-22 were detected by enzyme-linked immunosorbent assay (ELISA). Results The proportion of Th17 cells in AMI group and UA group ((2.98%±1.01%) and (2.63%±0.61%)), also the proportion of Th17/Th1 cells in AMI group and UA group ((0.71%±0.35%) and (0.66%±0.31%)), were both significantly higher than SA group and normal control group (both P<0.05) IL-17 and IL-22 concentration in AMI group (IL-17: 24.41±7.95 ng/L IL-22: 34.18±7.04 ng/L) were significantly higher than SA group and normal control group (both P<0.05). IL-17 concentration in UA group (22.86±8.62 ng/L) was significantly higher than normal control group IL-22 concentration in UA group (28.98±4.35 ng/L) was significantly lower than AMI group, significantly higher than normal control group. In ACS group, there was a significant positive correlation between IL-17 concentration and IL-22 concentration (r0.422, P<0.01), also there was a significant positive correlation between the proportion of Th17 cells and IL-17 concentration(r0.722, P<0.01), IL-22 concentration(r0.400, P<0.01). Conclusions Th17 cells may be involved in the incidence of the atherosclerotic plaque instability and ACS. IL-17 and IL-22 can be used as a secondary detection of ACS diagnosis.
ZHUO Yu-Feng , XU Ding-Li , CHENG Ying , HUANG Bing-Sheng , XIE Qiang , and LIN Gui-Xiong
2013, 21(04):341-344.
Abstract:Aim To investigate the differences of 40 mg versus 10 mg atorvastatin on the levels of serum prostacyclin and platelet activation in patients with ischemic cardiomyopathy (ICM).Methods 77 patients with ICM in the Department of Cardiology were recruited to this study from March 2008 to June 2010. Patients were randomly divided into two groups: 10 mg/d atorvastatin group (n38) and 40 mg/d atorvastatin group (n39). All subjects were followed up for 1 year. The levels of serum glutamic-pyruvic transaminase, creatine kinase, lipids, platelet, platelet activating factor (PAF), 6-keto-prostaglandin F1α(6-Keto-PGF1α) and thromboxane B2 (TXB2) were examined in all subjects at baseline and at the end of study. The incidences of adverse reactions in two study groups were taken down.Results At the end of this study, the levels of serum total cholesterol, low density lipoprotein cholesterol, TXB2, TXB2/6-Keto-PGF1α, PAF were significantly decreased and 6-Keto-PGF1α were significantly increased in 40 mg/d atorvastatin group in comparison with 10 mg/d atorvastatin group (P<0.05). There were no significant differences between the two groups on the levels of serum glutamic-pyruvic transaminase, creatine kinase, platelet and the incidences of adverse reactions for medicines.Conclusions 40 mg/d atorvastatin might significantly decrease the levels of platelet activation and increase the levels of serum prostacyclin in patients with ICM in comparison with 10 mg/d atorvastatin.
ZHENG Wei-Feng , ZHAO Luo-Sha , WEI Jing-Han , CHEN Qing-Hua , and DU You-You
2013, 21(04):345-348.
Abstract:Aim To observed the efficacy of Escitalopram joint Tandospirone in treating older women patients with coronary heart disease complicating anxiety disorder combined depression disorder.Methods The 100 older women patients with coronary heart disease complicating anxiety disorder combined depressio.disorder selected as the research object,were randomly divided into treatment group (50 cases) and the control group (50 cases). Hamilton anxiety scale (HAMA) and Hamilton depression scale (HAMD) were used to evaluate severity entrants of anxiety and depression of the patients. The changes of anxiety depression rating scale,angina pectoris,arrhythmia and acute myocardial infarction occurred situation before and after treatment in patients,drug safety,etc were observed.Results After Escitalopram joint Tandospirone treating in older women patients with coronary heart disease complicating anxiety disorder combined depression disorder based on routine treatment,the HAMA scores reducion was significantly higher in treatment group (14.07±5.39) than that in control group (7.19±4.81 P<0.05) The HAMD scores reducion were significantly higher in treatment group (14.59±6.76)than that in control group (7.28±6.27 P<0.05). The recurrence rate of coronary heart disease angina adverse events including angina pectoris,acute myocardial infarction,severe arrhythmia were 4.54%,0%,6.82% respectively in treatment group,they were 16.28%,2.33%,18.60% in control group,the coronary heart disease events of the treatment group were significantly lower than those in control group (P<0.05),and the drug safety was better.Conclusions Additional treatment of Escitalopram joint Tandospirone in older women patients with coronary heart disease complicating anxiety disorder combined depression disorder,may obtain a better benefit,improve the recovery.
LI Ping,JIANG Ran-Hua , LI Ling , LI Xue,LIU Cong , and YANG Fan
2013, 21(04):349-353.
Abstract:Aim To examine the association of adiponectin with metabolic syndrome (MS) and related cardiovascular disease (CVD) risk factors in Chinese adolescents.Methods This was a cross-sectional study including 933 adolescents. All participants underwent anthropometric and biochemical examinations. Adiponectin was measured using ELISA. The association of adiponectin with CVD risk factors and the presence of metabolic syndrome were evaluated. MS was defined with the International diabetes federation (IDF) 2007 definition specific for children and adolescents. Of the 933 subjects,the data of 907 ones were complete and entered the statistic analysis.Results With the reducing adiponectin,waist circumference (WC),body mass index (BMI),triglyceride (TG),hemoglobin A1c (HbA1c),fasting plasma insulin (FINS) and the homeostasis assessment model of insulin resistance (HOMA-IR) were increased (all P<0.05). Adiponectin was significantly correlated with WC,BMI,diastolic blood pressure (DBP),TG,total cholesterol (TC) and HbA1c (all P<0.05). Adiponectin showed independent association with MS (OR5.83,95% CI 1.98-17.18) and the most closely correlated component was central obesity (OR3.48,95%CI 1.84~6.59)and lower high density lipoprotein cholesterol (HDLC,OR1.57,95%CI 1.09~2.26).Conclusions Adiponectin was independently associated with the presence of MS and related multiple CVD risk factors in Chinese adolescents.
GUO Shou-Dong , YU Yang , FENG Lei , LIU Shuai , LI He-Lou , CUI Ying-Jie , and QIN Shu-Cun
2013, 21(04):354-358.
Abstract:Aim To establish a simplified extraction method from biological sample, and quantify sphingosine 1-phosphate (S1P) at the level of nanogram.Methods The methanol precipitation combing with ultrasonic extraction method was used to extract and separate S1P, then the supernatant was analyzed by liquid chromatography mass spectrometry (LC-MS) under the selective ion monitoring mode.Results The extraction method was effective and time saving, the limitation of quantification of S1P was 159.7 pg The S1P content in human plasma was 128.8 ± 33.3 μg/L, and the S1P content in plasma, heart, liver, lung, kidney and brain of the C57 BL/6 mouse was 181.8 ± 21.1 μg/L, 37.6 ± 2.8 ng/g, 54.9 ± 4.9 ng/g, 230.1 ± 60.5 ng/g, 21.5 ± 6.7 ng/g and 102.2 ± 23.8 ng/g, respectively.Conclusion Methanol precipitation combing with ultrasonic extraction could effectively separate S1P from plasma and organ, and the extract could be quantified by LC-MS directly. This method is effective with good reproducibility, and is suitable for quick quantitative analysis of a great deal of biological sample.
TANG Shu-Neng , ZHENG Jiang-Hua , MO Xiao-Hui , and WANG Ji-Ping
2013, 21(04):359-363.
Abstract:Aim To prepare and identify the monoclonal antibodies against recombinant protein of chlamydial protease-like activity factor from chlamydia pneumoniae for clinical diagnosing C.pneumoniae infection. Methods The chlamydial protease-like activity factor recombinant protein was used as antigen for the immunization of female BALB/c mice, and the spleen cells of mice were fused with SP2/0 myelomas. Indirect ELISA and Western blot analysis were used to screen the hybridomas secreting antibodies and then subcloning positive clones were carried out to establish stable cell lines by limiting dilution. Ascites were induced to produce MAbs and their specificity were identified by indirected immunofluorescence (IIF) test and Western blot analysis based C.pneumoniae type strain. The new indirect ELISA was estabilished to examine coronary artery plaques from patients and the results were analyzed by statistical method. Results Four hybridoma cell lines secreted the monoclonal antibodies stably were finally obtained and named as 3F8、7B9、8C4 and 11B5, respectively the subtype of the monoclonal antibodies secreted by 3F8 and 7B9 strain was IgG2b, the other two monoclonal antibodies were IgG1 and their titers in ascites were 1∶28000, 1∶16000, 1∶38000 and 1∶12000, respectively. The Western blot and IIF analysis showed that these monoclonal antibodies have excellent specificity to C.pneumoniae. The results of detecting clinical samples by the new indirect ELISA based on self-produced the monoclonal antibodies had better consistency with the results of PCR kits for C.pneumoniae infection. Conclusion The specific monoclonal antibodies against chlamydial protease-like activity factor recombinant protein of C.pneumoniae were obtained. All the 4 monoclonal antibodies belonged to IgG, which can react with native chlamydial protease-like activity factor from C.pneumoniae. The self-producted monoclonal antibodies are suitable for C.pneumoniae antigen diagnosis to coronary arteriosclerosis patients.
2013, 21(04):364-368.
Abstract:Berberine is a kind of traditional Chinese medicine of treating gastrointestinal diseases. With the deepening of the research, it has been found that berberine has an important role in the prevention of coronary heart disease. Therefore, the study of berberine has become one of the focuses in research of atherosclerosis. The effect of anti-atherosclerosis of berberine and its mechanism were reviewed from regulating lipid, resistant endothelial injury, anti-inflammatory response and antithrombotic in this article.
LIU Yan-Hui , and WEI Dang-Heng
2013, 21(04):369-374.
Abstract:Atherosclerosis is a chronic inflammation disease, which is determined by the interaction of environment factors and genetic factors. Epigenetic modification may be the bridge to link environment factors and genetic factors which contribute to the formation and progression of atherosclerosis. The deeper-knowledge of epigenetic modification such as DNA methylation, histone modification and micro RNA in atherosclerosis may further explore the mechanisms of atherosclerosis. Moreover, epigenetic modification is reversible, which may provide new therapeutic strategies and targets for atherosclerosis.
2013, 21(04):375-380.
Abstract:Percutaneous coronary intervention (PCI) is a mature therapeutic option in the treatment of coronary heart disease, which have significantly improved myocardial perfusion, the quality of life and reduced morbidity and mortality in patients with ischemic heart diseases in recent years. However, PCI can not only bring benefits to patients, but also cause irreversible mechanical damage of the intimal, eventually resulting in endothelial damage and restenosis of the target vessel. Although the strong effects of antiplatelet drugs and drug-eluting stent postoperative can reduce the rate of restenosis after stent implantation, late stent thrombosis and restenosis still can not be ignored. Adverse cardiac events after PCI continue to be problematic despite advances in stent design and adjunctive pharmacotherapy.The elucidation of the mechanism of PCI associated vascular injury may help to develop an effective treatment modality to manage the complications associated with PCI.
YANG Yan-Kun , SUN Xin , and ZHENG Hong
2013, 21(04):381-384.
Abstract:Vascular endothelial dysfunction plays an important role in the pathogenesis of atherosclerosis. As a protective barrier of vascular endothelium, glycocalyx plays a series of protection role, including regulation of vascular permeability, mediating the release of nitric oxide (NO) induced by shear stress, inhibition of the adhesion between leukocytes, platelets and endothelial cells, anticoagulation. This article reviews the important meaning of glycocalyx’s integrity and its endothelial protection, and its relationship with atherosclerosis.
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