Yan Guo

Beijing University of Chinese Medicine and Pharmacology, Peping, Beijing, China

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Publications (19)50.82 Total impact

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    ABSTRACT: Mai is the important concept in TCM and this term has been found in the early classic work of TCM. With the development and perfection of TCM theory, the original meaning of mai is "blood vessels entirely distrusted in the body". In five dynasties, the meaning of it was supplemented as "distribution of qi and blood in five zang and six fu organs to the four extremities", in which, not only blood but also qi has been included. With the constant understanding on mai, qi and blood, the unique concept of meridian and collateral is gradually generated. In terms of the modern study on the original meaning of mai and the academic evolution of meridian and collateral, it is discovered that qi is predominated and distributed in meridian and collateral as compared with blood. It is very significant to study the original meaning and academic evolution of mai, as well as the origin of the concept of meridian and collateral and to provide the reference support for the terminology standardization and basic study.
    No preview · Article · Oct 2015 · Zhongguo zhen jiu = Chinese acupuncture & moxibustion
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    ABSTRACT: Objective . To explore the effect of electroacupuncture (EA) on gene expression in the hypothalamus of rats with stress-induced prehypertension and try to reveal its biological mechanism with gene chip technology. Methods . The stress-induced hypertensive rat model was prepared by combining electric foot-shocks with generated noise. Molding cycle lasted for 14 days and EA intervention was applied on model + EA group during model preparation. Rat Gene 2.0 Array technology was used for the determination of gene expression profiles and the screened key genes were verified by real-time fluorescence quantitative PCR method. Results . Compared with the blank group, 234 genes were upregulated and 73 were downregulated in the model group. Compared with the model group, 110 genes were upregulated and 273 genes were downregulated in model + EA group. The PCR results of the key genes including HSPB1, P2RX4, PPP1R14A, and TH are consistent with that of gene chip test. Conclusion . EA could significantly lower blood pressure of stress-induced prehypertension rats and affect its gene expression profile in hypothalamus. Genes and their signal transduction pathway that related to the contraction of vascular smooth muscle, concentration of Ca 2+ , and excitability of sympathetic nerve may be involved in EA’s antihypertensive mechanism.
    Preview · Article · Aug 2015 · Evidence-based Complementary and Alternative Medicine
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    ABSTRACT: To explore electro-acupuncture's (EA's) effect on gene expression in heart of rats with stress-induced pre-hypertension and try to reveal its biological mechanism based on gene chip technology. Twenty-seven Wistar male rats were randomly divided into 3 groups. The stress-induced hypertensive rat model was prepared by electric foot-shocks combined with generated noise. Molding cycle lasted for 14 days and EA intervene was applied,on rats in model + EA group during model preparation. Rat Gene 2.0 Sense Target Array technology was used for the determination of gene expression profiles and the screened key genes were verified by real-time quantitative polymerase chain reaction (RT-PCR) method. Compared with blank control group, 390 genes were changed in model group; compared with model control group, 330 genes were changed in model+EA group. Significance analysis of gene function showed that the differentially expressed genes are those involved in biological process, molecular function and cellular components. RT-PCR result of the screened key genes is consistent with that of gene chip test. EA could significantly lower blood pressure of stress-induced pre-hypertension rats and affect its gene expression profile in heart. Genes that related to the contraction of vascular smooth muscle may be involved in EA's anti-hypertensive mechanism.
    Preview · Article · Jun 2015 · Journal of Traditional Chinese Medicine
  • Min Fang · Junhong Wang · Shiling Li · Yan Guo
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    ABSTRACT: The current study was carried out to evaluate the effect of advanced glycation end-products (AGE) on cardiac aging and to explore its underlying mechanisms. Neonatal rat cardiac fibroblasts were cultured and divided into four groups: control; AGE; AGE + receptor for AGE antibody and AGE + SB431542 (transforming growth factor-β [TGF-β]/Smad signaling pathway inhibitor, 10 μmol/L) group. After being cultured for 48 h, the cells were harvested and the senescence-associated beta-galactosidase expression was analyzed. Then the level of p16, TGF-β, Smad/p-smad and matrix metalloproteinases-2 was evaluated by western blot. Significantly increased senescence-associated beta-galactosidase activity as well as p16 level was observed in the AGE group. Furthermore, AGE also significantly increased the TGF-β1, p-smad2/3 and metalloproteinases-2 expression in cardiac fibroblasts (all P < 0.01). Meanwhile, either pretreatment with receptor for AGE-Ab or SB431542 significantly inhibited the upregulated cardiac senescence (beta-galactosidase activity and P16) and fibrosis-associated (TGF-β1, p-smad2/3 and metalloproteinases-2) markers induced by AGE. Taken together, all these results suggested that AGE are an important factor for cardiac aging and fibrosis, whereas the receptor for AGE and TGF-β/Smad signaling pathway might be involved in the AGE-induced cardiac aging process. Geriatr Gerontol Int 2015; ●●: ●●-●●. © 2015 Japan Geriatrics Society.
    No preview · Article · May 2015 · Geriatrics & Gerontology International
  • Junhong Wang · Bo Tang · Xinjian Liu · Xin Wu · Hui Wang · Di Xu · Yan Guo
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    ABSTRACT: Background: Monomeric CRP (mCRP) plays an important role in the process of atherosclerotic plaque rupture. Recently, it has been reported that mCRP was associated with acute myocardial infarction (AMI). Objectives: The aim of this study was to examine whether mCRP is increased in AMI patients and to investigate the possibility of using circulating mCRP as a biomarker for AMI diagnosis and severity assessment of disease. Methods: A mCRP monoclonal antibody was generated and verified for its specificity. Immunofluorescence was used to assess the localization of mCRP in the infarcted myocardium. Furthermore, 101 AMI, 38 unstable angina pectoris (UAP) and 41 stable angina pectoris (SAP) patients were enrolled, and 43 healthy volunteer were recruited as controls in the study. Venous blood samples were collected to measure the circulating mCRP, cardiac Troponin T and hs-CRP levels. Results: Significantly increased mCRP levels were observed in the infarcted myocardium of model mice. In addition, significantly increased plasma mCRP levels were also detected in AMI patients (20.96±1.64ng/ml) compared to those with UAP, SAP or in control patients (all 0ng/ml, p<0.001). ROC analysis revealed that circulating mCRP had considerable diagnostic accuracy for AMI with an AUC of 0.928 (95% confidence interval 0.887-0.969). Furthermore, nine patients (9/101, 8.91%) in AMI group died before the 30-day follow-up, and their plasma mCRP concentration was significantly higher than those in surviving patients (36.70±10.26 vs. 19.41±1.43ng/ml, P=0.002). Conclusions: These results indicate that mCRP is increased in AMI and that circulating mCRP might be a potential biomarker for diagnosis and severity assessment of disease in AMI.
    No preview · Article · Apr 2015 · Atherosclerosis
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    ABSTRACT: The aim of this paper was to explore the long-term effects and pain relief mechanism of acupuncture knife on third lumbar vertebrae (L3) transverse process syndrome. Forty SD rats were randomized into control, model, electroacupuncture (EA), and acupuncture knife (AK) group. Except control rats, other rats were subjected to an operation to emulate L3 transverse process syndrome. Fourteen days after the operation, EA and AK rats were given electroacupuncture and acupuncture knife treatments, respectively. Fifty-six days after the operation, enzyme-linked immunosorbent assay was used to measure substance P (SP), 5-hydroxytryptamine (5-HT), interleukin-1β (IL-1β), interleukin-10 (IL-10), tumor necrosis factor-α (TNF-α), and transforming growth factor-β (TGF-β) in peripheral blood. The tail flick test was used to observe pain threshold. We found that rats with the simulation operation had significantly higher levels of SP, 5-HT, IL-1, IL-10, TNF-α, and TGF-β, while the AK rats had lower levels. In addition, the pain threshold of AK rats was similar to that of control rats. AK pretreatment could alleviate pain through modulating inflammatory response.
    Preview · Article · Dec 2014 · Evidence-based Complementary and Alternative Medicine
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    ABSTRACT: Prostaglandin E2 (PGE2) has been implicated in cell invasion in hepatocellular carcinoma (HCC), via increased β1-integrin expression and cell migration; however, the mechanism remains unclear. PGE2 exerts its effects via four subtypes of the E prostanoid receptor (EP receptor 1-4). The present study investigated the effect of EP1 receptor activation on β1-integrin expression and cell migration in HCC. Cell migration increased by 60% in cells treated with 17-PT-PGE2 (EP1 agonist), which was suppressed by pretreatment with a β1-integrin polyclonal antibody. PGE2 increased β1-integrin expression by approximately 2-fold. EP1 receptor transfection or treatment with 17-PT-PGE2 mimicked the effect of PGE2 treatment. EP1 siRNA blocked PGE2-mediated β1-integrin expression. 17-PT-PGE2 treatment induced PKC and NF-κB activation; PKC and NF-κB inhibitors suppressed 17-PT-PGE2-mediated β1-integrin expression. FoxC2, a β1-integrin transcription factor, was also upregulated by 17-PT-PGE2. NF-κB inhibitor suppressed 17-PT-PGE2-mediated FoxC2 upregulation. Immunohistochemistry showed p65, FoxC2, EP1 receptor and β1-integrin were all highly expressed in the HCC cases. This study suggested that PGE2 upregulates β1-integrin expression and cell migration in HCC cells by activating the PKC/NF-κB signaling pathway. Targeting PGE2/EP1/PKC/NF-κB/FoxC2/β1-integrin pathway may represent a new therapeutic strategy for the prevention and treatment of this cancer.
    No preview · Article · Oct 2014 · Scientific Reports
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    ABSTRACT: The rapidly activating delayed rectifier potassium current (IKr) plays a critical role in cardiac repolarization. Although IKr is known to be regulated by both α1- and β1-adrenergic receptors (ARs), the cross-talk and feedback mechanisms that dictate its response to α1- and β1-AR activation are not known. In the present study, IKr was recorded using the whole-cell patch-clamp technique. IKr amplitude was measured before and after the sequential application of selective adrenergic agonists targeting α1- and β1-ARs. Stimulation of either receptor alone (α1-ARs using 1 μM phenylephrine (PE) or β1-ARs using 10 μM xamoterol (Xamo)) reduced IKr by 0.22 ± 0.03 and 0.28 ± 0.01, respectively. The voltage-dependent activation curve of IKr shifted in the negative direction. The half-maximal activation voltage (V0.5) was altered by -6.35 ± 1.53 and -1.95 ± 2.22 mV, respectively, with no major change in the slope factor (k). When myocytes were pretreated with Xamo, PE-induced reduction in IKr was markedly blunted and the corresponding change in V0.5 was significantly altered. Similarly, when cells were pretreated with PE, Xamo-induced reduction of IKr was significantly attenuated. The present results demonstrate that functional cross-talk between α1- and β1-AR signaling regulates IKr. Such non-linear regulation may form a protective mechanism under excessive adrenergic stimulation.
    Preview · Article · Aug 2014 · International Journal of Molecular Sciences
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    ABSTRACT: To examine the association between hemoglobin (Hb) levels and cardiovascular risk factors in a large community-dwelling cohort. A total of 4,186 women and 4,851 men were enrolled in the study. Data on personal history, physical examination and biochemical parameters were collected. Subjects were categorized by gender and divided into different group according to the level of Hb or blood pressure, and the association between Hb levels and cardiovascular risk factors was examined using Pearson's correlation analysis. In both men and women even with normal Hb level, tertiles of Hb levels were positively associated with body mass index (BMI), total-cholesterol (TC), triglyceride (TG), uric acid (UA), diastolic blood pressures (DBP) and fasting plasma glucose (FPG) (all P=0.000 in men and women). Furthermore, significantly increased incidence of hyperuricemia (P=0.000 both in men and women) and obesity (P=0.000 both in men and women) were observed with the gradually increased Hb level. In addition, Pearson's correlation analysis revealed obvious correlation between Hb level and various cardiovascular risk factors including blood pressure and UA. Binary logistic regression analysis further demonstrated that the level of Hb was an important risk factor for elevated blood pressure (OR =1.216; 95% CI: 1.138-1.293, P=0.000 in men; OR =1.287; 95% CI: 1.229-1.363, P=0.000 in women). Increasing Hb levels, even in subjects with normal level were associated with increasing prevalence of cardiovascular risk factors, suggesting that a slightly low Hb level might be beneficial to Chinese community-dwelling individuals.
    No preview · Article · May 2014 · Journal of Thoracic Disease
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    ABSTRACT: To explore the long-term effects and pain relief mechanism of acupotomy by observing changes in nitric oxide synthase (NOS) and beta-endorphin (beta-EP) in the hypothalamus, spinal cord, and peripheral blood of rats with third lumbar vertebrae (L3) transverse process syndrome. Twenty-eight SD rats were randomly assigned to normal, model, electroacupuncture (EA), and acupotomy group. The last three groups were put through an operation to emulate L3 transverse process syndrome. Fourteen days after the simulation operation, EA and acupotomy treatments were applied to the respective groups. Fifty-six days after the simulation operation, biochemistry tests and enzyme-linked immunosorbent assay were used to measure NOS and beta-EP in the hypothalamus, spinal cord, and peripheral blood. Rats with the simulation operation showed significantly higher levels of NOS and beta-EP in the hypothalamus, spinal cord, and peripheral blood than those in the normal group. The EA and acupotomy groups had significantly lower levels of NOS and beta-EP than those in the model group. There was no statistical difference between the EA and acupotomy groups. EA and acupotomy treatments significantly lowered NOS and beta-EP levels in the hypothalamus, spinal cord, and peripheral blood and alleviated L3 transverse process syndrome.
    No preview · Article · Apr 2014 · Journal of Traditional Chinese Medicine
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    ABSTRACT: Background: Guinea pig ventricular cardiomyocytes display the rapid component of the delayed rectifier potassium current (Ikr) that contributes to ventricular repolarization and promotes stress-induced arrhythmias. Adrenergic stimulation favors ventricular arrhythmogenesis but its effects on Ikr are poorly understood. Methods: Adrenergic modulation of Ikr was studied in isolated guinea pig ventricular cardiomyocytes using whole-cell patch clamping. Results: We found that the Ikr amplitude was reduced to 0.66±0.02 and 0.62±0.03 in response to 0.1 µM phenylephrine (PE), an α1AR agonist, and 10 µM isoproterenol (ISO), a βAR agonist, respectively. The effect of PE can be blocked by the selective α1A-adrenoceptor antagonist 5-methylurapidil, but not by the α1B-adrenoceptor antagonist chloroethylclonidine or α1D-adrenoceptor antagonist BMY7378. Additionally, the effect of ISO can be blocked by the β1-selective AR antagonist CGP-20712A, but not by the β2-selective AR antagonist ICI-118551. Although PE and ISO was continuously added to cells, ISO did not decrease the current to a greater extent when cells were first given PE. In addition, PE's effect on Ikr was suppressed by β1AR stimulation. Conclusions: Ikr can by regulated by both the α1 and β ARs system, and that in addition to direct regulation by each receptor system, crosstalk may exist between the two systems.
    Preview · Article · Mar 2014 · Molecular Medicine Reports
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    ABSTRACT: No available prognostic factor was identified for atherosclerotic renovascular stenosis (ARAS) patient who undergo the percutaneous revascularization therapy. This is a case of 68-year-old ARAS patient associated with hypertension and massive proteinuria, who exhibited progressive aggravation of renal dysfunction. His proteinuria selectivity index (SI) was only 0.08. Then the stenosis was treated by percutaneous transluminal angioplasty of the renal artery (PTRA) and stenting. After 2-year follow up, all symptoms including renal dysfunction and uncontrolled hypertension was well-controlled. As no reliable predictors of clinical response have been identified yet, SI might be a simple prognositic index for ARAS patients undergone the revascularzation therapy.
    No preview · Article · Aug 2013 · Journal of Thoracic Disease
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    ABSTRACT: The prostaglandin E2 (PGE2) EP1 receptor has been implicated in hepatocellular carcinoma (HCC) cell invasion. However, little is known about the mechanisms of EP1 receptor-mediated cell adhesion and migration. We previously showed that PGE2 promotes cell adhesion and migration by activating focal adhesion kinase (FAK). The present study was designed to elucidate the association between the EP1 receptor and FAK activation in HCC cells and to investigate the related signaling pathways. The effects of PGE2, EP1 agonist 17-phenyl trinor-PGE2 (17-PT-PGE2), PKC and EGFR inhibitors on FAK activation were investigated by treatment of Huh-7 cells. Phosphorylation of FAK Y397 and c-Src Y416 was investigated by western blotting. Cell adhesion and migration were analyzed by WST and transwell assays, respectively. Protein kinase C (PKC) activity was measured with a PKC assay kit. The results showed that 17-PT-PGE2 (3 µM) increased FAK Y397 phosphorylation by more than 2-fold and promoted cell adhesion and migration in Huh-7 cells. In transfected 293 cells, expression of the EP1 receptor was confirmed to upregulate FAK phosphorylation, while the EP1 receptor antagonist sc-19220 decreased PGE2-mediated FAK activation. PKC activity and c-Src Y416 phosphorylation were enhanced after 17-PT-PGE2 treatment. Both PKC and c-Src inhibitor suppressed the 17-PT-PGE2-upregulated FAK phosphorylation, as well as 17-PT-PGE2-induced cell adhesion and migration. In addition, exogenous epidermal growth factor (EGF) treatment increased FAK phosphorylation. The EGF receptor (EGFR) inhibitor also suppressed 17-PT-PGE2-upregulated FAK phosphorylation. Our study suggests that the PGE2 EP1 receptor regulates FAK phosphorylation by activating the PKC/c-Src and EGFR signal pathways, which may coordinately regulate adhesion and migration in HCC.
    Preview · Article · Mar 2013 · International Journal of Oncology
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    ABSTRACT: Liver cancer is a common human cancer with a high mortality rate and currently there is no effective chemoprevention or systematic treatment. Recent evidence suggests that prostaglandin E2 (PGE2) plays an important role in the occurrence and development of liver cancer. However, the mechanisms through which PGE2 promotes liver cancer cell growth are not yet fully understood. It has been reported that the increased expression of FUSE-binding protein 1 (FBP1) significantly induces the proliferation of liver cancer cells. In this study, we report that PGE2 promotes liver cancer cell growth by the upregulation of FBP1 protein expression. Treatment with PGE2 and the E prostanoid 3 (EP3) receptor agonist, sulprostone, resulted in the time-dependent increase in FBP1 protein expression; sulprostone increased the viability of the liver cancer cells. The protein kinase A (PKA) inhibitor, H89, and the adenylate cyclase (AC) inhibitor, SQ22536, inhibited the cell viability accelerated by sulprostone. By contrast, the Gi subunit inhibitor, pertussis toxin (PTX), exhibited no significant effect. Treatment with PGE2 and sulprostone caused a decrease in JTV1 protein expression, blocked the binding of JTV1 with FBP1, which served as a mechanism for FBP1 degradation, leading to the decreased ubiquitination of FBP1 and the increase in FBP1 protein expression. Furthermore, H89 and SQ22536 prevented the above effects of JTV1 and FBP1 induced by PGE2 and sulprostone. These findings indicate that the EP3 receptor activated by PGE2 may couple to Gs protein and activate cyclic AMP (cAMP)-PKA, downregulating the levels of JTV1 protein, consequently inhibiting the ubiquitination of FBP1 and increasing FBP1 protein expression, thus promoting liver cancer cell growth. These observations provide new insights into the mechanisms through which PGE2 promotes cancer cell growth.
    Preview · Article · Jan 2013 · International Journal of Oncology

  • No preview · Article · Nov 2012 · International journal of cardiology
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    ABSTRACT: The aim of the present study was to make use of the artificially induced aging model cardiomyocytes to further investigate potential anti-aging-associated cellular diastolic dysfunction effects of EGB761 and explore underlying molecular mechanisms. Cultured rat primary cardiomyocytes were treated with either D-galactose or D-galactose combined with EGB761 for 48 h. After treatment, the percentage of cells positive for SA-β-gal, AGEs production, cardiac sarcoplasmic reticulum calcium pump (SERCA) activity, the myocardial sarcoplasmic reticulum calcium uptake, and relative protein levels were measured. Our results demonstrated that in vitro stimulation with D-galactose induced AGEs production. The addition of EGB761 significantly decreased the number of cells positive for SA-β-gal. Furthermore, decreased diastolic [Ca(2+)](i), curtailment of the time from the maximum concentration of Ca(2+) to the baseline level and increased reuptake of Ca(2+) stores in the SR were also observed. In addition, the level of p-Ser16-PLN protein as well as SERCA was markedly increased. The study indicated that EGb761 alleviates formation of AGEs products on SERCA2a in order to mitigate myocardial stiffness on one hand; on other hand, improve SERCA2a function through increase the amount of Ser16 sites PLN phosphorylation, which two hands finally led to ameliorate diastolic dysfunction of aging cardiomyocytes.
    Full-text · Article · May 2012 · Oxidative Medicine and Cellular Longevity
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    ABSTRACT: J Clin Hypertens (Greenwich). 2012;14:245–249. ©2012 Wiley Periodicals, Inc. Atorvastatin is postulated to improve arterial stiffness in patients with diabetes mellitus or hypercholesterolemia; however, in elderly hypertensive patients, its effect on arterial stiffness and the possible mechanisms are unknown. A total of 73 elderly hypertensive patients were enrolled to receive atorvastatin for 6 months. Brachial-ankle pulse wave velocity (baPWV) and circulating biomarkers were measured before and after the intervention. After 6 months of treatment, the patients experienced a 19.66% reduction in low-density lipoprotein cholesterol (2.90±0.58 vs 2.33±0.56 mmol/L, P<.01) and a 10.63% reduction in baPWV (2100.89±513.21 vs 1877.56±432.06 cm/s, P=.01). In addition, a 21.79% reduction in circulating N-(epsilon)-carboxymethyl-lysine and a 20% reduction in Von Willebrand factor level were observed after treatment. Meanwhile, the activity of copper/zinc-containing superoxide dismutase (Cu/Zn SOD) was increased by 26.64% (5.04±1.01 vs 6.87±1.83 U/L, P<.001). Correlation analysis demonstrated that the increase of Cu/Zn SOD activity was related to the reductions of arterial stiffness (r=−0.340, P=.003). Taken together, these findings suggest that atorvastatin can improve arterial stiffness possibly by reducing oxidative stress levels in elderly hypertensive patients.
    Full-text · Article · Apr 2012 · Journal of Clinical Hypertension
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    ABSTRACT: Metabolic syndrome (MetS) is regarded as a risk factor for coronary artery disease (CAD). But the influence of MetS on morbidity and mortality after stent implantation in CAD patients remains unknown. This article presents a meta-analysis of available data on the association between the MetS and the risk of angiographic and clinical outcomes following stent implantation. MetS was associated with a significant increased risk of post-stent all-cause mortality (odd ratio (OR), 2.17, 95% CI, 1.56-3.01), in-lesion restenosis (OR, 1.35, 95% CI, 1.00-1.84) and major adverse cardiac events (MACE) (OR 1.35, 95% CI 1.13-1.61) in CAD patients. Even with drug-eluting stent (DES) implantation, significant increased risk in all-cause mortality (OR, 2.25, 95% CI, 1.61-3.15) and MACE (OR 1.42, 95% CI 1.14-1.76) were remain in patients with MetS. However, the OR of cardiovascular (CV) mortality (1.25, 95% CI 0.71-2.22), MI (1.27, 95% CI 0.87-1.85) and TLR (OR 1.21, 95% CI 0.96-1.53) was not statistically different between the patients with and without metabolic syndrome. Metabolic syndrome is an important risk factor in patients with CAD following stent implantation. Although DES implantation decreased the incidence of angiographic events, further progress in adequate treatment of MetS is still required to improve the clinical outcome.
    No preview · Article · Dec 2011 · Atherosclerosis
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    ABSTRACT: The literature provides no clear answer as to whether matrix metalloproteinases (MMPs) polymorphisms increases risk of myocardial infarction (MI). Our purpose was to help clarify the inconsistent findings of MMPs polymorphisms and MI susceptibility and identify which MMP polymorphism might play an active role in the occurrence of MI. Articles were identified by a Medline search and citation tracking. Eligible articles were case-control studies of MMPs polymorphisms and MI which met our prespecified criteria. Data were independently extracted by two authors according to a predefined protocol. Incongruities were settled by consensus decision. 18 potentially eligible articles were identified. In a combined analysis, the 5A allele of the MMP-3 5A/6A polymorphism was associated with MI (OR 1.21, 95% CI 1.01 to 1.46, p=0.04), suggesting its role in plaque rupture. In the subgroup analysis by ethnicity, significantly increased risk was found among East Asians (OR 1.39, 95% CI 1.01 to 1.91, p=0.04), whereas no significant association was detected in Caucasian populations. In addition, there were significant associations of the MMP-9 -1562C→T polymorphism with MI (OR 1.14, 95% CI 1.02 to 1.27, p=0.02), whereas the heterogeneity of the studies showed no significance (I(2)=13.7%, p=0.32). This meta-analysis demonstrated that the MMP-3 5A/6A and MMP-9 -1562 C→T polymorphisms are risk factors associated with increased MI susceptibility, but these associations vary in different ethnic populations.
    Preview · Article · Oct 2011 · Heart (British Cardiac Society)
  • Yan Guo · Miao Lu · Jin Qian · Yun-lin Cheng
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    ABSTRACT: To investigate the possible effects of alagebrium chloride (ALT-711) on oxidative stress (OS) process in aging hearts, we examined the role of ALT-711 in cardiac function and OS in the heart of aging rats. Increased mitochondrial DNA (mtDNA) deletion as well as nearly a twofold increase in advanced glycation end products (AGEs) accumulation were observed in aging heart, whereas only about 50% of the superoxide dismutase (SOD) and glutathione peroxidase (GSH-PX) activities were seen. However, after treatment with ALT-711, preserved cardiac diastolic function accompanied with reduced mtDNA deletion and about 30% of AGEs decrease was observed in aging hearts. In addition, ALT-711 can increase SOD and GSH-PX activities in aging hearts as well as in cultured cardiomyocytes. In conclusion, our study suggests that AGEs accumulation and the abnormalities in the OS in aging hearts can be attenuated by ALT-711, and this might be a novel underlying mechanism for ALT-711 in the treatment of cardiovascular diseases that develop with aging.
    No preview · Article · Apr 2009 · The Journals of Gerontology Series A Biological Sciences and Medical Sciences

Publication Stats

84 Citations
50.82 Total Impact Points

Institutions

  • 2014-2015
    • Beijing University of Chinese Medicine and Pharmacology
      Peping, Beijing, China
  • 2011-2015
    • Nanjing Medical University
      Nan-ching, Jiangsu, China