2012, 20(10):865-870.
Abstract:High density lipoprotein(HDL)is not a homogeneous category of lipoproteins, different HDL subclasses have distinct but complementary metabolic function.Alterations in plasma lipid and apolipoprotein levels can interfere with the distribution of HDL subclasses that affect atherosclerosis risk.The general shift toward smaller size of HDL particle size in hypertriglyceridemia (HTG), hypercholesteromia (HCL) and mixed hyperlipidemia (MHL) subjects, and the changes were more prominent with the elevation of TG and TC levels which imply that HDL maturation might be abnormal and reverse cholesterol transport (RCT) pathway might be weakened, and these changes were more serious in MHL subjects.Apolipoproteins have distinct but interrelated roles in HDL particles generation and metabolism.As the concentration of apoAⅠ increases, the contents of all HDL subclasses increase significantly.The most significant association was observed between large-sized HDL2b contents and apoAⅠ.ApoAⅡ played a dual function in the contents of HDL subclasses, and both small-sized HDL3b and HDL3a and large-sized HDL2b tended to increase with apoAⅡ concentration.Plasma apoB-100, apoCⅡ, and apoCⅢ appear to play a coordinated role in assembly of HDL particles and the determination of their contents.Higher concentrations of apoAⅠ could inhibit the reduction in content of large-sized HDL2b affected by apoB-100, CⅡ, and CⅢ.The particle size of HDL tend to be small in diabetes and CHD patients.For CHD patients with statins therapy, the HDL subclasses phenotype modification lagged behind the improvement of plasma lipids levels.The HDL subclasses distribution may help in severity of coronary artery and risk stratification, especially in CHD pa-tients with therapeutic low density lipoprotein (LDL), triglyceride(TG) and HDL levels.
WEN Yu , YANG Shan-Shan , LIU Jing , HU Xiu-Fen
2012, 20(10):871-875.
Abstract:AimTo examine the effect of estradiol, testosterone and progesterone on Visfatin gene and protein expression in cultured 3T3-L1 adipocytes and preadipocytes.Methods0 mmol/L (sex hormones-free DMEM/F12), 10-8 mol/L, 10-7 mol/L and 10-6 mol/L estradiol or testosterone or progesterone were added to cultured 3T3-L1 adipocytes or preadipocytes overnight.Total RNA and proteins were extracted.Then the expression of Visfatin mRNA and protein was measured by RT-PCR and Western blot, respectively.ResultsOvernight incubation with estradiol increased Visfatin mRNA expression in both adipocytes (24% to 21%, p<0.05) at the concentration of 10-8 mol/L to 10-7 mol/L and preadipocytes (70% to 123%, p<0.01) at 10-7 mol/L to 10-6 mol/L, respectively.Visfatin mRNA expression increased by 28%(p<0.05) at 10-8 mol/L testosterone in adipocytes, 76% (p<0.05) at 10-7 mol/L testosterone in preadipocytes.Progesterone did not affect Visfatin mRNA expression on adipocytes, but had a marked increase in Visfatin expression in preadipocytes by 2.6-fold (p<0.05).In 3T3-L1 adipocytes, estradiol had small but insignificant effects on Visfatin protein expression, whereas testosterone had a much greater effect, increasing Visfatin protein by 134% at 10-6 mol/L (p<0.05).However, progesterone significantly decreased Visfatin protein by 32% at 10-6 mol/L (p<0.05).ConclusionsThese data suggest that Visfatin may play a physiological role in the insulin resistance caused by estradiol, testosterone or progesterone in 3T3-L1 adipocytes and preadipocytes.
XU Yan , LIU Hai-Mei , XU Jin-Wen , JIANG Ping , WANG Ting-Huai
2012, 20(10):876-880.
Abstract:AimTo investigate the effects of 17β-estradiol on myocardial hypertrophy induced by testosterone, and to explore the role of ERK1/2 protein in the signal transduction pathway of sexual hormone in development of myocardial hypertrophy.MethodsMyocardial cells were isolated from ventricles of 1~3-day-old neonate rats purified by a culture method based on Simpson.Neonate rat cardiomyocyte hypertrophic responses were assayed by measuring protein content, protein synthesis rate.Expression of protein ERK1/2 was detected by Western blot.Results17β-estradiol (E2) was able to inhibit the increase of cell protein and 3H-Leu incorporation induced by T in a range from 10-10~10-6 mol/L, with an optimal concentration of 10-8 mol/L.The effect of E2 was partly intercepted by Tamoxifen.The inhibitory effect of E2 on the increase of 3H-Leu incorporation in cardiomyocytes induced by testosterone was not enhanced by PD98059.The increased expression of ERK1/2 induced by testosterone was reversed by E2 at concentration of 10-8 mol/L.The increased expression of ERK1/2 induced by testosterone which was inhibited by E2 was reversed by pretreating with Tamoxifen (10-6 mol/L) for 2 h.ConclusionE2 could reverse the myocardial hypertrophy induced by testosterone by inhibiting the expression of ERK1/2, which was mediated by estrogen receptor.
SHAN Hai-Yan , BAI Xiao-Juan , Wang He-Zhi , CHEN Xiang-Mei
2012, 20(10):881-884.
Abstract:AimTo investigate the role of Valsartan on Angiotensin Ⅱ(AngⅡ)-induced senescence of human umbilical endothelial cell senescence and gene expression of p16INK4a.MethodsHUVEC were cultured in vitro and intervened by AngⅡ(10-6mol/L) and Valsartan(AngⅡ type 1 receptor blocker).HUVEC were divided into 3 groups, the control group, AngⅡ group, Valsartan group.β-gal staining was used to identify cell aging status.Flow cytometry was used for analyzing the cell cycle changes; The positive cell rate of p16INK4a was detected by immunocytochemical staining, and the expressions of p16INK4a protein were determined by Western blot.ResultsCompared with the control cells, the positive cell number of β-gal staining was significantly higher in AngⅡ-induced cells 81.24%±6.46%; the cell cycle was at G0-G1 88.36%±6.45%. In Valsartan group, p16INK4a protein expression decreased evidently (p<0.05) compared to that in the AngⅡ group, which suggests that p16INK4a activity plays an important role in regulating vascular endothelial cell senescence lifespan in vitro.ConclusionCell Endothelial cell senescence is induced by AngⅡ.One of its molecular mechanisms might be associated with increasing the expression level of p16INK4a in aging cell, and then up-regulating the amount of cells blocking in G1 phase of cell cycle.Valsartan could antagonize the process effectively and delay endothelial cell aging significantly.
ZHAO Lan , ZHANG Shao-Heng , YAN Jian
2012, 20(10):885-889.
Abstract:AimTo investigate the expressions of protein kinase B (Akt) and stromal cell-derived factor-1 (SDF-1) and their relations with circulating blood endothelial progenitor cell homing after myocardial infarction (MI).MethodsMI was induced in the Sprague-Dawley (SD) rats by left anterior descending artery ligation.Akt inhibitor or dimethyl sulfoxide (DMSO) was injected into an ischemic zone. At 1, 7, 14 and 28 days post-MI, the expression of Akt and SDF-1 in the infarcted hearts were determined by enzyme-linked immunosorbent assay (ELISA).Circulating blood endothelial progenitor cells (EPCs) or ischemic myocardial EPCs was evaluated by flow cytometry analysis (FACS) or immunohistochemistry (IH).The number of vessels was examined by IH.ResultsELISA showed that the expression levels of Akt and SDF-1 increased gradually during the early stages of acute ischemia, and reached the highest levels by 14 days post-MI.Similar to the response of Akt and SDF-1 to myocardial ischemia, FACS and IH revealed the same changes of circulating blood EPCs or myocardial EPCs, and blood vessel counting displayed the same dynamic changes.The changes of these observed indices were markedly blocked by Akt inhibitor, which showed no significant difference between all the individual time-points after MI.ConclusionIschemic myocardiocytes post-MI may regulate homing of circulating blood EPCs, survival of stem cells, and angiogenesis of the infarcted hearts by Akt-SDF-1 signal pathway.
LI Jun , WANG Guo-Rong , WANG Yan , XIE Yan-Ying , MU Yan-Ling , YAO Qing-Qiang
2012, 20(10):890-894.
Abstract:AimTo investigate the effects of tetrahydroxystilbene glucoside (TSG) on monocyte chemoattractant protein-1 (MCP-1), intercellular cell adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) mRNA expression of human umbilical vein endothelial cells (HUVEC) injuored by homocysteine (Hcy).MethodsHUVEC were treated with different concentration of TSG for 2 hours then treated with Hcy.Cell nucleus damage was detected by Hoechst33342 stain.mRNA expression levels of MCP-1, ICAM-1 and VCAM-1 were detected by RT-qPCR.ResultsPreincubation with TSG could attenuate the nucleolus damage of HUVEC induced by Hcy.While TSG concentration is less than 10 μmol/L, TSG showed a concentration dependent in decreasing the damage of Hcy on HUVEC.TSG decreased MCP-1, ICAM-1 and VCAM-1 mRNA expression that were increased by Hcy in HUVEC.ConclusionMCP-1, ICAM-1 and VCAM-1 mRNA expressions which were increased by Hcy in HUVEC in vitro can be reduced by TSG
LU Qiong , HE Jin , ZHOU Zhi-Gang , MENG Jun , TU Jian , TU Yu-Lin
2012, 20(10):895-898.
Abstract:AimTo observe the effect of Amlodipine on the expression of platelet-derived growth factor-B(PDGF-B) and nuclear factor-κB (NF-κB) in human umbilical vein endothelial cell (HUVEC-12) induced by oxidized low density lipoprotein (ox-LDL), further to explore the related mechanism of Amlodipine through its role on ox-LDL/NF-κB/PDGF-B.MethodsAfter pretreated with different concentration (0, 0.1, 1.0, 10.0 μmol/L) of Amlodipine for 0.5 h and treated with 50 mg/L ox-LDL for 24 h, the expressions of PDGF-B and NF-κB protein were respectively detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western Blot.Then, Pyrrolidinedithiocarbamic acid, ammonium salt(PDTC), a kind of NF-κB inhibitor was added, and RT-PCR and Western Blot were used to detect the expression of PDGF-B and NF-κB.ResultsWith the increasing concentration of Amlodipine, the PDGF-B and NF-κB protein expressions were all down-regulated obviously.PDTC not only down-regulated the NF-κB protein expression, but also the PDGF-B expression, as effectively as 10.0 μmol/L Amlodipin group.ConclusionAmlodipine can down-regulate the PDGF-B expression in HUVEC-12 induced by ox-LDL through NF-κB.
YANG Zheng , QIU Min , GUO Xiao-Hua , LI Jun-Ping , CHEN Li-Zhu , SUN Shu-Yan
2012, 20(10):899-902.
Abstract:AimTo investigate the effect of extractive of pericarpium trichosanthis (EPT) on cell cycle of rat vascular smooth muscle (VSMC) proliferation induced by platelet-derived growth factor-BB (PDGF-BB) and to probe especially into its mechanism.MethodsVSMC from the thoracic aorta of SD rats were cultured by tissue explant method.Effect of EPT (10, 20 and 30 mg/L) on PDGF-BB-induced VSMC proliferation was assessed by 3H-TdR method, the cell cycle was analyzed by flow cytometry, expression of c-fos and c-myc mRNA in VSMC were detected by real-time quantitative reverse transcription-polymerase chain reaction (real-time RT-PCR).ResultsPDGF-BB could significantly increase the rate of 3H-TdR incorporation (p<0.01) and the percentage of S phase cells, and degrade the G0/G1 phase cell percentage in the cell cycle (p<0.01).At the same time, PDGF-BB could up-regulate c-fos and c-myc mRNA expression (p<0.01).Addition of EPT (10, 20 and 30 mg/L) markedly inhibited the PDGF-BB-induced proliferation of the VSMC (p<0.01), decreased the S phase cell percentage and upgraded the G0/G1 phase cell percentage in the cell cycle, EPT could also depress the elevated expression of c-fos and c-myc mRNA indcued by PDGF-BB.ConclusionsEPT could inhibit the VSMC proliferation induced by PDGF-BB through preventing the transformation of the G0/G1 phase cell to S phase cell in the cell cycle.The mechanism may be related to its down-regulatory effect on c-fos and c-myc mRNA expressions.
QU Run-Bo , LU Yu-Sa , GONG Fei-Yu
2012, 20(10):903-907.
Abstract:AimTo observe the intervention of atorvastatin on myocardial energy metabolism in rabbits with hypercholesterolemia.MethodsTwenty-four male New Zealand white rabbits were randomly divided into three groups:control group,cholesterol group, atorvastatin treated group fed with cholesterol.After feeding for 6 weeks,the empty stomach blood preparation through ear marginal vein were collected,the levels of serum total cholesterol were determined;the myocardium was taken to observe its ultrastructures by electron microscopy;High-performance liquid chromatography (HPLC) was used to measure myocardial mitochondria ATP and CoQ10;Ultraviolet spectrophotomtry was used to measure the activities of SDH and CCO.ResultsIn cholesterol group there were myocardial fibers derangement,part of the fracture,dissolution,mitochondria swelling,crest disturbance,fuzzy, and Comparing with control group,the activities of SDH and CCO were significantly decreased,the content of myocardial mitochondria ATP and CoQ10 was significantly decreased(p<0.01).Compared with cholesterol group, the activities of SDH and CCO in atorvastatin treated group were increased(p<0.01), and comparing the content of myocardial mitochondria ATP and CoQ10, there was no significant difference between the two groups (p>0.05).ConclusionsAtorvastatin may reduce structure damage of myocardial mitochondrial cause by hypercholesterolemia,increase the activities of SDH and CCO,thereby improve the oxidative phosphorylation capacity of mitochondrial.
WU Lian-Pin , CHEN Gan , GAO Xue-Zhong , LIU Gan , Aili·Maihemuti
2012, 20(10):908-910.
Abstract:AimTo study clinical effects of Shenmai injection on unstable angina and understand its mechanism.Methods178 cases with unstable angina, was divided into treatment group and control group.Treatment group was treated by conventional western medicine plus ShenMai injection.The control group was treated by conventional western medicine plus GIK injection.Observe symptoms of angina and ECG remission situation and detect the plasma tissue factor pathway inhibitor-2 concentration before and after treatment.ResultsThe clinical baseline was similar.Symptom remission rates of treatment group and control group were 84.3%, 69.7%;ECG improvement rates was 74.5%,61.8%.There were significant differences (p<0.05).The plasma tissue factor pathway inhibitor-2 declined after treatment.But the treatment group decreased more significantly; the difference was significant (p<0.01).ConclusionsThe Shenmai injection plus the conventional western medicine can effectively alleviate the unstable angina.Its treatment effect may be related to the changes of tissue factor pathway inhibitor-2.
GUO Tai-Lin , ZHU Peng-Li , LIN Fan , YU Hui-Zhen , HONG Fu-Yuan , ZHANG Li
2012, 20(10):911-914.
Abstract:AimTo explore the relationship between ankle-brachial index (ABI) and arterosclerosis in patients with non-dialysis chronic kidney disease (CKD).MethodsAs a cross-sectional study, 118 patients with diagnosis of non-dialysis CKD (stage 1-5) were selected in our hospital from October 2008 to October 2009.Clinical data were recorded, including sex, age, height, weight, smoking status, blood pressure (BP), fasting glucose, high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC) and renal function.Estimated glomerular filtration rate (eGFR) was calculated by Modification of Diet in Renal Disease Study equation.ABI values were determined with a Dopper prober.ResultsAccording to eGFR, all patients were divided into 5 groups as CKD stage 1 group to CKD stage 5 group.Compared with CKD stage 1 group, ABI values were significantly decreased in CKD stage 3 group, stage 4 group and stage 5 group (all p<0.01).There was no difference between CKD stage 1 group and stage 2 group (p>0.05).ABI value was significantly decreased with gradual decline of eGFR level (p<0.01).Multiple regression analysis showed that age, diabetes, hypertension and eGFR were risk factors for the ABI value (p<0.01).ConclusionsRenal dysfunction is an independent risk factor for arterosclerosis. Decline of eGFR was closely related with the degree of arterosclerotic lesions. ABI can be used as important clinical indicators of arterosclerosis in patients with CKD.
TAO Li-Hua , FENG Tian-Yuan , JIANG Zhong-Hua , ZHUANG Guo-Hua , HUANG Cheng-Lin , WANG Jian
2012, 20(10):915-917.
Abstract:AimTo explore the relationship of serum endothelial lipase and macrovascular complications in type 2 diabetes patients (T2DM).Methods66 patients with type 2 diabetes were divided into macrovascular complications group and no macrovascular complications group.30 cases of healthy persons were used as control group.Fasting serum endothelial lipase levels were measured with enzyme linked immunosorbent assay ( ELISA) and compared between groups.ResultsThe serum endothelial lipase in type 2 diabetes with macrovascular complications (3.31±1.30 ng/L) was significantly higher than that of no macrovascular complications group(2.54±1.11 ng/L) and control group (2.36±0.91 ng/L,p<0.05).No macrovascular complications group had no significant differences from the control group.Related analysis showed that the serum endothelial lipase in type 2 diabetes was positively correlated with glycosylated hemoglobinA1c( HbA1c) and high sensitive C-reactive protein ( hs-CRP), and negatively correlated with high-density lipoprotein (HDL).ConclusionsEndothelial lipase might be involved in the occurrence and development of macrovascular lesions in type 2 diabetes patients.
HU Xiao-Yan , XIAO Zhi-Jie , LIU Han-Rui , CHANG Bo , QIN Wei
2012, 20(10):918-922.
Abstract:AimTo explore the relationship between the lipoprotein lipase (LPL) -447C/G gene polymorphism and cerebral infarction in the elderly.MethodsThis was a case-control study, which enrolled 206 cases with cerebral infarction in the elderly and 203 elderly incerebrovascular disease controls.The genotype and allele frequencies of lipoprotein lipase-447C/G gene polymorphism were assayed by polymerase chain reaction-restricted fragment length polymorphism (PCR-RFLP).The cerebral infarction patients were strictly diagnosed according to revise conference in the national fourth session of cerebrovascular disease.The basic document object of study was collection through questionnaire interview.ResultsThe LPL-447C/G genotype and allele distribution in the cerebral infarction group was CC 83.98%, CG+GG 16.02% and C 91.75%, G 8.25% respectively.The distribution in control group was CC 81.77%, CG+GG 18.23% and C 90.89%, G 9.11% respectively.There was no significant difference in LPL-447C/G allele and genotype distribution between the cerebral infarction group and the control group (p>0.05).There was no significant difference detected in blood pressure level and blood lipids level between various genotypes (p>0.05).Cerebral infarction multi-factor regression equation indicated primary hazard factors included smoking history, diabetes history and family history.Conclusions(1)LPL-447C/G gene polymorphism is not significantly associated with cerebral infarction in elderly.(2)LPL-447C/G gene polymorphism is not significantly associated with blood lipids level, blood pressure level in elderly.
WANG Ming-Sheng , LIN Jian-Ying
2012, 20(10):923-926.
Abstract:AimTo observe the impact of Shuxuening on the clinical effects and quality of life in old patients with ischemic stoke.Methods212 old patients with ischemic stroke were randomly divided into study group and control group.The control group was treated with conventional therapy; the study group was treated with Shuxuening additionally.All were treated for 2 weeks.The nerve function deficit score was evaluated, SS-QOL table was used to evaluate the quality of life in patients, the level of endothelin-1 (ET-1) and calcitonin gene related peptide(CGRP) were recorded.ResultsAfter treatment, the clinical efficiency were 86.8% in study group and 76.5% in control one(p<0.05); for the study group, the score of SS-QOL and CGRP increased greatly,ET-1 decreased greatly, and there were significant difference between the two groups (p<0.05 or p<0.01).ConclusionCombined with conventional therap, Shuxuening could improve the nerve function deficit score and quality of life in old patients with ischemic stoke.
2012, 20(10):927-930.
Abstract:AimTo contrast inflammatory level and safety of different doses atorvastatin (lipitor) treatment group, and to find basis for lipid-drugs to use in acute ST-segment elevation myocardial infarction (STEMI) reasonably.Methods111 patients with STEMI were divided into two groups according to different doses of atorvastatin after percutaneons coronary intervention: 40 mg/d treatment group, 20 mg/d treatment group.The therapeutical effect was tested including inflammatory factors,lipid-level and UCG of preoperative and postoperative 1 month, and including hepatic function and renal function of preoperative and postoperative 1 month.ResultsThe lipid-lowering,anti-inflammatory,improving left venticular function of atorvastatin 40 mg treatment group were better than the atorvastatin 20 mg treatment group, but the side effect had no difference between the two groups.ConclusionsIn China, atorvastatin 40 mg/d in STEMI after percutaneons coronary intervention may be safe and effective.
ZHAO Ji-Hong , LIANG Guo-Qing , ZHOU Bing-Wei , JIANG Tie-Min
2012, 20(10):931-933.
Abstract:AimTo discuss the clinical significance of the plasma levels of homocysteine (Hcy) and C-reactive protein(CRP) combined with ankle brachial index(ABI) to the assessment of the severity of peripheral artery lesions in patients with peripheral arterial disease(PAD).MethodsThe plasma levels of Hcy and CRP combined with ABI were test in patients(n=86) with PAD confirmed by selective peripheral angiography,and in the normal control group(n=80).Relationship between the severity of peripheral artery lesions with the plasma levels of Hcy and CRP combined with ABI was analysed.ResultsCompared with the normal control group, the plasma levels of Hcy and CRP in PAD group were significantly higher than those of the normal control group(p<0.05 and p<0.01),and ABI was significantly lower (p<0.01).In PAD group, the plasma levels of Hcy and CRP in multi-vessel disease sub-group were significantly higher than in single-vessel disease sub-group(p<0.01 and p<0.05), and ABI was significantly lower(p<0.01).ConclusionsThe plasma levels of Hcy and CRP combined with ABI are related to the severity of peripheral artery lesions, which has the important guiding value to evaluate the clinical condition.
ZHANG Yi-Jun , PEI Jing-Xian , WU Ping-Sheng
2012, 20(10):934-938.
Abstract:AimTo evaluate the differences of the changes of arterial stiffness of hypertension patients with the treatment of calcium channel blocker (CCB) or angiotensin Ⅱ receptor blocker (ARB).MethodsBased on the principles of evidence-based medicine, corresponding inclusion and exclusion criteria, along with search strategies were developed.We searched the Ovid EMB Reviews, Pubmed, EMBASE, Chinese Biomedical Literature Database, Chinese Scientific Journal Full-text Database, and Chinese Journal Full-text Database up to January 2012 to identify randomized controlled trials (RCT) comparing the effects of CCB with that of ARB on arterial stiffness of hypertension patients.Two reviewers independently evaluated the quality of the included studies, extracted data with a unified form, and analyzed the data by Cochrane Collaboration’s RevMan 5.0 software.We compared the effects of CCB with ARB on pulse wave velocity (PWV), SBP, DBP and PP of hypertension patients.ResultsSix RCT involving 411 paitents were included.The results of Meta analysis suggested that ARB was better than CCB in reducing arterial stiffness (MD=183.33, 95%CI was 79.32~ 287.33), but worse than CCB in lowering SBP (MD=-2.66, 95%CI was -3.35 ~-1.96) or DBP (MD=-5.43, 95%CI was -8.8~-2.07).ConclusionIn the treatment of anti-hypertension, CCB is stronger than ARB.But the effect of ARB is better than that of CCB on reducing arterial stiffness.And it’s not related to their antihypertensive function.However, due to the quality of the included studies, the effects of CCB and ARB on arterial stiffness need to be confirmed by large multicenter randomized controlled trials.
2012, 20(10):939-944.
Abstract:AimThe endoplasmic reticulum (ER) is an organelle involved in protein folding, calcium homeostasis, and lipidbiosynthesis.Various factors that interfere with ER function disrupt ER homeostasis,which result in ER stress.The unfolded protein response(UPR) is initiated to adapt to the changing environment, and reestablish normal ER homeostasis.Prolonged and excessive ER stress triggers cell suicide, usually in the form of apoptosis, and plays an important role in many diseases.It is found in recent studies that ER stress is involved in the pathogenesis of injured vascular diseases such as atherosclerosis, hypertension, vascular calcification, and restenosis.Here, we reviewed recent progresses in ER stress and injured vascular diseases.
2012, 20(10):945-950.
Abstract:Paraoxonase-3 (PON3) is a member of the paraoxonase (PON) family.In addition to PON3, it also includes PON1 and PON2.They share a large number of structural homology, and all the three proteins prevent oxidative stress and fight inflammation.They therefore seem central to a wide variety of human illnesses, including atherosclerosis, obesity, diabetes, inflammation bowel disorders and mental disorders.In vitro studies, the antioxidant capacity of PON3 is even stronger than PON1, so PON3 may also have the potential to become the treatment factors of certain diseases.The purpose of this review is to conclude some of the latest findings on PON3 in recent years, so as to provide new ideas for further research of the PON family.
WANG Li-Li , WANG Hong-Yan , QU Peng
2012, 20(10):951-955.
Abstract:Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs) are two major pattern-recognition receptors (PRRs) in the early host defence against pathogen invasion, TLRs are expressed on plasma membranes, whereas NLRs are in the cytosol.They through the cause of sterile inflammation and synergy participate in the occurrence and development of atherosclerosis, bridge the innate immunity and arteriosclerosis.
TANG Wei-Liang , PENG Fang , WANG Xing-Xiang , Guo Hang-Yuan
2012, 20(10):956-960.
Abstract:The patients after coronary stent implantation requires regular dual antiplatelet therapy with aspirin and clopidogrel.When these patients are complicated with indications for anticoagulation therapy, such as atrial fibrillation, left ventricular thrombosis and so on, the triple antithrombotic therapy combined with aspirin, clopidogrel and warfarin is usually employed.However, because of significant bleeding risk of this treatment, clinicians are puzzled with its safety, effectiveness and necessity, and researchers currently debate this as a hot spot.In this paper, we have reviewed the recent literatures about the triple antithrombotic therapy, and discussed the application of this treatment in patients with coronary heart disease.
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