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Backgrounds The Systemic Immune-Inflammation Index (SII), as a novel inflammatory biomarker, has not been researched for type 2 diabetes mellitus (T2DM). This study was designed to investigate the potential association between SII and T2DM. Methods This cross-sectional study focused on adults enrolled in 2011 and 2018 by National Health and Nutrition Examination Survey (NHANES). Univariate, as well as multivariate logistic regression analyses, subgroup analyses, and sensitivity analyses, were performed to determine the independent association between SII and T2DM. The relationship between ln-SII and T2DM was described by the fitted smoothing curve. Results A total of 10,321 subjects were enrolled in the study; of which 2,078 (20.1%) were diagnosed with T2DM. After full adjustment, multivariate logistic regression demonstrated that higher SII was an independent risk factor for increased T2DM (OR = 1.30; 95% CI, 1.08–1.56, p

Acute myocardial infarction (AMI) is a common cause of death worldwide and heart failure (HF) is the main complication. Although the increase in percutaneous coronary intervention and drug treatment can reduce in-hospital mortality after AMI, the incidence of HF after AMI and the resulting risk of death are still rising, which causes difficulties in the rehabilitation of AMI patients after reperfusion.In this prospective, multicenter, randomized, double-blind, double-dummy, placebo-controlled trial, we will assigned 673 eligible patients with AMI after reperfusion into 4 groups: receiving Nao-Xin-Tong capsule (NXT), Bu-Yang-Huan-Wu (BYHW) granule (BYHW), Yang-Yin-Tong-Nao granule (YYTN), or placebo. The course of treatment will be 3 months. The primary outcome is HF incidence within 180 days. Nao-Xin-Tong capsule, BYHW granule, and Yang-Yin-Tong-Nao granule are different traditional Chinese medicines used for tonifying Qi and activating blood (TQAB).Three months of TQAB combined with Western medicine may reduce the incidence of HF after reperfusion of AMI and improve patients' quality of life.This study will provide an important basis for the application of traditional Chinese medicine in patients with AMI after reperfusion and provide an evidence-based basis for the prevention and treatment strategy of HF after AMI.

Objective: To explore the possible mechanism for the treatment of NRR in arrhythmia by using network pharmacology and molecular docking in this study. Methods: Active compounds and targets for NRR were retrieved from the Traditional Chinese Medicine Systems Pharmacology (TCMSP) Database and Analysis Platform, SymMap, and also from the Encyclopedia of Traditional Chinese Medicine (ETCM) databases. Arrhythmia-related genes were acquired from the Comparative Toxicogenomics Database (CTD) and the GeneCards database. Overlapping targets of NRR associated with arrhythmia were acquired and displayed via a Venn diagram. DAVID was applied for GO and KEGG pathway analyses. Cytoscape software and its plug-in were used for PPI network construction, module division and hub nodes screening. AutoDock Vina and qRT-PCR were carried out for validation. Results: In total, 21 active compounds and 57 targets were obtained. Of these, coumarin was the predominant category which contained 15 components and 31 targets. There were 5 key targets for NRR in relation to treating arrhythmia, and these targets are involved in the apoptotic process, extrinsic apoptotic signaling pathway in absence of ligand, endopeptidase activity involved in apoptotic process by cytochrome c. The main pathways were p53 signaling pathway, Hepatitis B and apoptosis. The results from the molecular docking and qRT-PCR displayed good effects on hub node regulation in NRR treatment. Conclusion: NRR plays an important role in anti-apoptotic mechanisms mediated by modulating p53 signaling pathway, which may provide insight for future research and clinical applications focusing on arrhythmia therapy.

To assess the trends in characteristics, treatments, and outcomes of acute myocardial infarction (AMI) patients in tertiary Chinese medicine (CM) hospitals in China between 2006 and 2013. This retrospective study was based on two nationwide epidemiological surveys of AMI in tertiary CM hospitals during 2 years (2006 and 2013). Patients admitted to the hospital for AMI were enrolled. Hospital records were used as the data source. Case data were derived regarding baseline characteristics, treatments, and outcomes of patients to assess changes from 2006 to 2013. Logistic regression was used to analyze the relationship between prognosis, general influencing factors of disease, and various treatment measures. Totally 26 tertiary CM hospitals in 2006 and 29 tertiary CM hospitals in 2013 (18 were repetitive) were surveyed. A total of 2,311 patients with AMI were enrolled (1,094 cases in 2006 and 1,217 cases in 2013). From 2006 to 2013, the mean age did not significantly change, but the proportion of patients younger than 65 years increased. The prevalence of risk factors such as hypertension, diabetes, and hyperlipidemia also increased. Significant increases were observed in primary percutaneous coronary intervention [20.48% (2006) vs. 24.90% (2013)] and revascularization [36.11% (2006) vs. 52.42% (2013)]. In-hospital mortality decreased from 11.15% in 2006 to 10.60% in 2013. A mortality logistic regression analysis identified reperfusion therapy [odds ratio (OR), 0.222; 95% confidence interval (CI), 0.106–0.464], Chinese patent medicines (OR, 0.394; 95% CI, 0.213–0.727), and CM decoctions (OR, 0.196; 95% CI, 0.109–0.353) as protective factors. Reperfusion and revascularization capabilities of tertiary CM hospitals have improved significantly, but in-hospital mortality has not significantly decreased. Efforts are needed to improve medical awareness of AMI and expand the use of CM to reduce in-hospital mortality in China.

Objectives. We aimed to investigate the effects of Shen-Yuan-Dan (SYD), a Chinese medicine preparation, on periprocedural myocardial injury (PMI) and the number of peripheral blood endothelial progenitor cells (EPCs) in patients with unstable angina pectoris (UA) who underwent elective percutaneous coronary intervention (PCI). Methods. Patients were randomly divided into the experimental (group A) and control (group B) groups through the random number table method. In group A, patients concurrently received the conventional western treatment and SYD orally (4 capsules/time, 3 times/d, from 3 d before surgery to 7 d after surgery). In group B, patients received conventional Western medicine treatment. Both groups underwent coronary angiography, and patients undergoing PCI were eventually included in the study. The following patient data were collected: incidence of PMI, serum CK-MB content before PCI, 4 h, 24 h, and 7 d after PCI, number of CD45dim/-CD34+CD309+ peripheral venous EPCs, and number of CD184 coexpressed EPCs. The incidence of adverse reactions and 30-day major adverse cardiovascular events (MACEs) were also recorded. Results. Sixty-two patients were finally included in this study, with 32 and 30 in groups A and B, respectively. In group A, the number of peripheral blood EPCs and the number of CD184 coexpressed EPCs at 1 h before surgery were higher than those at 3 d before surgery (37.24 ± 25.20 vs. 22.78 ± 9.60/ml; P < 0.001 and 23.38 ± 15.30 vs. 13.54 ± 8.08/ml; P < 0.001 , resp.). The number of peripheral blood EPCs and number of CD184 coexpressed EPCs at 4 h after surgery were lower than those at 1 h before surgery (25.30 ± 11.90 vs. 37.24 ± 25.20/ml; P = 0.019 and 15.38 ± 8.78 vs. 23.38 ± 15.30/ml; P = 0.013 , resp.), but there was no difference at 24 h and at 7 d after surgery in comparison with that at 1 h before surgery ( P > 0.05 ). In group B, compared with that at 1 h before surgery, there existed a decline in the number of EPCs in peripheral blood and the number of CD184 coexpressed EPCs at 4 h after surgery, but without a statistical difference ( P > 0.05 ). Comparing both groups, it was found that the incidence of PMI in group A was lower (6.25% vs. 26.67%; P = 0.04 ), and the serum CK-MB content at 4 and 24 h after surgery was also lower than that in group B (17.33 ± 5.83 vs. 20.38 ± 4.32 U/l; P = 0.048 and 15.79 ± 5.32 vs. 19.10 ± 4.93 U/l; P = 0.030 , resp.). The number of EPCs in peripheral blood and the number of CD184 coexpressed EPCs in group A were higher than those in group B at 1 h before surgery (37.24 ± 25.20 vs. 22.36 ± 12.26/ml; P = 0.034 and 23.38 ± 15.30 vs. 13.12 ± 14.62/ml; P = 0.013 , resp.). In addition, there were no obvious adverse reactions and no 30-day MACEs in both groups during the trial. Conclusion. SYD can reduce PMI and promote the mobilization of EPCs in the perioperative period of elective PCI in patients with UA.

Background Many experiments showed that Notopterygii Rhizoma Et Radix (NRR) can resist arrhythmia, but the mechanism of its action has not clear. Here, we investigated the possible mechanisms of NRR by network pharmacology and molecular docking and verified them experimentally. Methods Active componds and targets of NRR were retrieved by the Traditional Chinese Medicine Systems Pharmacology (TCMSP) Database andAnalysis Platform, SymMap, and the Encyclopedia of Traditional Chinese Medicine (ETCM) databases. Arrhythmia-related targets were acquired from Comparative Toxicogenomics Database (CTD) and GeneCards databases. Overlapping targets of NRR associated with arrhythmia were acquired via Venn diagram. DAVID was applied for GO and KEGG pathway analyses. Cytoscape software and its plug-in were used for PPI network construction, module division and hub nodes screening. AutoDock Vina and qRT-PCR were carried out for validation. Results The 21 active compounds and 57 targets were obtained. Of these, coumarin was the predominant category including 15 components and 31 targets. The 5 key targets of NRR in treating arrhythmia, and these targets are involved in the apoptotic process, extrinsic apoptotic signaling pathway in absence of ligand, endopeptidase activity involved in apoptotic process by cytochrome c. The main pathways are p53 signaling pathway, Hepatitis B and Apoptosis. The results of molecular docking and qRT-PCR display good effect on hub node regulation in NRR treatment. Conclusion NRR plays an important role in anti-apoptotic mediated by modulating p53 signaling pathway, which may provide insight into future research and clinical applications in arrhythmia therapy.

Background: Heart failure (HF) is the end stage of ischemic cardiovascular diseases; nonetheless, safe and effective therapeutic agents for HF are still lacking, and their discovery remains challenging. Our previous studies demonstrated that Shen-Yuan-Dan Capsule (SYDC), a hospital preparation of traditional Chinese herbal, effectively protected ischemic injury in cardiovascular diseases. However, its therapeutic effects and possible mechanisms on HF remain unclear.Methods: A zebrafish HF model treated with verapamil was developed to assess the therapeutic effect of SYDC on HF zebrafish. Zebrafish were administered with SYDC and digoxin (positive control) by direct soaking. After drug treatment, zebrafish were randomly assigned to the visual observation and image acquisition using a Zebralab Blood Flow System. The reactive oxygen species (ROS), MDA, and SOD levels were determined by fluorescence signal detection, TBA, and WST-8 methods. RT-PCR determined the mRNA expressions of Caspase-3, Caspase-1, Bcl-2, Bax, IL-1β, NF-κB, and TNF-α.Results: SYDC significantly inhibited the levels of heart dilatation and venous congestion and markedly increased the levels of cardiac output, blood flow dynamics, and heart rates in HF zebrafish (p < 0.05, p < 0.01, and p < 0.001). Moreover, SYDC also significantly decreased the levels of MDA and ROS and increased the level of SOD in HF zebrafish. The RT-PCR results revealed that SYDC decreased the expression of Caspase-1, Caspase-3, Bax, IL-1β, NF-κB, and TNF-α but increased the expression of Bcl-2 in HF zebrafish (p < 0.05, p < 0.01, and p < 0.001).Conclusions: SYDC improved the heart function in verapamil-induced HF zebrafish and alleviated inflammation and apoptosis by inhibiting the ROS-mediated NF-κB pathway.

Background/Aim. Danhong injection (DHI) is a Chinese patent drug used for relieving cardiovascular diseases. Recent studies have suggested that DNA methylation plays a pivotal role in the maintenance of cardiac fibrosis (CF) in cardiovascular diseases. This study was aimed at identifying the effect and the underlying mechanism of DHI on CF, especially the DNA methylation. Methods. A CF murine model was established by thoracic aortic constriction (TAC). A 28-day daily treatment with or without DHI via intraperitoneal injection was carried out immediately following TAC surgery. The changes in cardiac function, pathology, and fibrosis following TAC were measured by echocardiography and immunostaining. We used methyl-seq analysis to assess the DNA methylation changes in whole genes and identified the methylation changes of two Ras signaling-related genes in TAC mice, including Ras protein activator like-1 (Rasal1) and Ras-association domain family 1 (Rassf1). Next, the methylation status and expression levels of Rasal1 and Rassf1 genes were consolidated by bisulfite sequencing, quantitative reverse transcription polymerase chain reaction (RT-qPCR), and Western blotting, respectively. To determine the underlying molecular mechanism, the expressions of DNA methyltransferases (DNMTs), Tet methylcytosine dioxygenase 3 (TET3), fibrosis-related genes, and the activity of Ras/ERK were measured by RT-qPCR and Western blotting. Results. DHI treatment alleviated CF and significantly improved cardiac function on day 28 of TAC. The methyl-seq analysis identified 42,606 differential methylated sites (DMSs), including 19,618 hypermethylated DMSs and 22,988 hypomethylated DMSs between TAC and sham-operated mice. The enrichment analysis of these DMSs suggested that the methylated regulation of Ras signal transduction and focal adhesion-related genes would be involved in the TAC-induced CF development. The results of bisulfite sequencing revealed that the TAC-induced methylation affected the CpG site in both of Rasal1 and Rassf1 genes, and DHI treatment remarkably downregulated the promoter methylation of Rasal1 and Rassf1 in CF hearts. Furthermore, DHI treatment upregulated the expressions of Rasal1 and Rassf1, inhibited the hyperactivity of Ras/ERK, and decreased the expressions of fibrosis-related genes. Notably, we found that DHI treatment markedly downregulated the expression of DNMT3B in CF hearts, while it did not affect the expressions of DNMT1, DNMT3A, and TET3. Conclusion. Aberrant DNA methylation of Rasal1 and Rassf1 genes was involved in the CF development. DHI treatment alleviated CF, prevented the hypermethylation of Rasal1 and Rassf1, and downregulated DNMT3B expression in CF hearts.

BACKGROUND: Moderate autophagy plays a positive role in the prevention of atherosclerosis. Aberrant promoter methylation of autophagic genes can affect autophagy. Shen-Yuan-Dan Capsule (SYDC), a traditional Chinese medicine, can prevent atherosclerosis in high-fat-fed mice. However, its precise mechanism remains unclear. This study investigated the mechanism of SYDC in ameliorating atherosclerosis in a mice model. METHODS: After 6 weeks of a high-fat diet, apolipoprotein E knockout (apoE(–/–)) mice were randomly grouped into control, Lipitor, and SYDC groups (n = 10). The mice were intragastrically administered with the respective drugs for 6 weeks. The expressions of Beclin1 and Atg5-Atg12 complex in atherosclerotic plaques of the mice were measured. The levels of 5-mC and DNA methyltransferase 1 (DNMT1) in the plasma of the mice were determined. The average methylation rate of CpG islands in the promoter region of autophagy-related protein (Atg13) and the mRNA expression of Atg13 in the aortas of the mice were determined. RESULTS: SYDC up-regulated the expressions of Atg5-Atg12 complex and Beclin-1 in atherosclerotic plaques (p < 0.01). Moreover, SYDC decreased the 5-mC and DNMT1 levels in plasma and atherosclerotic plaques of the mice (p < 0.01), and also decreased the average methylation rate of CpG islands in the promoter region of Atg13 and increased the mRNA levels of Atg13 in the aortas of atherosclerotic mice (p < 0.01). CONCLUSIONS: SYDC attenuates atherosclerosis by promoting autophagy, probably through regulating genomic DNA methylation and Atg13 promoter demethylation.

Background/aim Danhong injection (DHI) is a Chinese drug used for relieving cardiovascular diseases. This study aimed to identify the effect and mechanism of action of DHI on post-infarct angiogenesis, especially the epigenetic regulation of angiogenesis. Methods A myocardial infarction (MI) mouse model was induced by ligating the left anterior descending coronary artery. A 4-week daily treatment with or without DHI via intraperitoneal injection was started immediately following MI. The changes in cardiac function, pathology, and angiogenesis following MI were measured by echocardiography and immunostaining. Matrigel tube formation and scratch wound assays were used to evaluate the effect of DHI on the proliferation and migration of hypoxic human umbilical vein endothelial cells (HUVECs). The expression of miR-126, Spred-1, and angiogenesis-related mRNAs was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The expression of related proteins and the phosphorylated levels of extracellular signal–regulated kinase (ERK) and protein kinase B were detected by Western blot analysis. The loss-of-function study was performed using antagomir-126. Results The DHI-treated mice had significantly reduced infarct area, improved ejection fraction, and increased capillary density 4 weeks after MI. Also, DHI promoted the proliferation and migration of hypoxic HUVECs. The qRT-PCR and Western blot analysis revealed that DHI intervention upregulated miR-126, suppressed Spred-1 expression, and activated the ERK pathway, but not the Akt pathway. The loss-of-function study showed the blockade of the pro-angiogenic effect of DHI by antagomir-126 involving the ERK/vascular endothelial growth factor (VEGF) pathway. Conclusion DHI enhanced post-infarct angiogenesis after MI by activating the miR-126/ERK/VEGF pathway.

Background and aims High-fat diet (HFD) is reported to induce atherosclerosis and insulin resistance. Macrophage lipid accumulation has been implicated as key mediators during the development of HFD-induced atherosclerosis. Traditional Chinese formula, which has long been used to improve disorder of glucose and lipid metabolism of patients, is now gradually being used as complementary therapy. This study aimed to investigate the effect of Danhong injection (DHI), a Chinese medicine used for the treatment of coronary artery disease, on atherosclerosis and its underlying mechanisms. Methods and results We observed the effects of DHI on HFD-induced atherosclerosis in a mice model, macrophage lipid accumulation in an ox-LDL-stimulated macrophage model, and the role of PI3K/AKT insulin pathway in the process of DHI ameliorating atherosclerosis. The data demonstrated that DHI attenuated atherosclerosis by ameliorating blood lipids, reducing the atherosclerotic index and atherosclerotic plaque area in HFD-induced atherosclerotic mice, and inhibiting TC levels in an ox-LDL-induced macrophage model. By estimating the levels of serum insulin resistance-related indexes and protein expression of GLUT-4, DHI treatment dramatically inhibited the levels of fasting serum NEFA and fasting serum insulin and promoted the protein expression of GLUT-4 in aortas of the HFD-induced atherosclerotic mice. Moreover, according to the hints provided by microarray-based transcriptional profiling, the results demonstrated that DHI treatment also promoted the activation of PI3K/AKT insulin signaling pathway induced by IRS-1 in aortas of HFD-induced atherosclerotic mice. Furthermore, in an ox-LDL-induced macrophage model, the activation of PI3k/AKT signaling pathway also effectively functioned in the process of DHI inhibiting macrophage lipid accumulation. Conclusions These results highlight that DHI treatment attenuates atherosclerosis and macrophage lipid accumulation by promoting the activation of PI3K/AKT insulin signaling pathway. It provides new insights into the molecular mechanism of DHI and its therapeutic potential in the treatment of atherosclerosis.

Background and Aim: PI3K/Akt/mTORC1 signaling pathway plays a crucial role in autophagy. Autophagy acts as a negative regulator of inflammation. Our previous studies demonstrated that Shen-Yuan-Dan Capsule (SYDC), a Chinese medicine used for treating angina pectoris, has anti-atherosclerotic effects in mice model and exert anti-inflammatory activities. However, its effects on autophagy and PI3K/Akt/ mTORC1 signaling pathway remains unclear. This study aimed to explore the effect of SYDC on autophagy and PI3K/Akt/mTORC1 signaling pathway in ApoE-/- mice model and ox-LDL-induced macrophage-derived foam cell model to delineate the underlying mechanism. Methods: After 6 weeks of high-fat diet, ApoE/ mice were randomly grouped into control, Lipitor, low-SYDC (SYDC-L), middle-SYDC (SYDC-M), and high-SYDC (SYDC-H) groups (n= 10).The mice were intragastricly administered with the respective drug for 6 weeks. Murine RAW264.7 cells were stimulated with oxidized low-density lipoprotein (ox-LDL) (80 μg/ml) for 24 h and then pretreated with SYDC freeze-dried powder for another 24h. The cells treated by SYDC were co-cultured for 24 hours with LY294002, tricirbine and rapamycin to investigate the possible mechanisms of action. Results: SYDC ameliorated blood lipids, reduced atherosclerotic indexes and plaque areas in aortic root of atherosclerotic mice, and inhibited the total cholesterol (TC) levels and ChE/TC ratios in ox-LDL stimulated macrophages. Moreover, SYDC up-regulated the protein expressions of Beclin1 and LC3Ⅱ/Ⅰratios in aortas of the atherosclerotic mice and ox-LDL stimulated macrophages. Moreover, SYDC inhibited the protein expressions of AKT phosphorylation at Ser473, and mTOR phosphorylation at Ser2448 in aortas of the atherosclerotic mice and ox-LDL stimulated macrophages. Furthermore, the inhibitory effect on ChE/TC ratios of SYDC in ox-LDL stimulated macrophages can be abolished by the selective inhibition of the PI3K/Akt/mTORC1 signal pathway. Conclusions: Taken together, these results highlight that SYDC treatment attenuates foam cell formation by promoting autophagy via inhibiting the activation of PI3K/Akt/mTORC1 signaling pathway. It provides new insights into the molecular mechanism of SYDC and its therapeutic potential on the treatment of atherosclerosis.

Background: Peri-procedural myocardial injury (PMI) during percutaneous coronary intervention (PCI) will result in an unfavorable clinical prognosis in patients, thus urgently necessitating effective drug treatment measures. Shen-Yuan-Dan (SYD) capsules are a traditional Chinese medicine (TCM) preparation that have been found to have potential myocardial protection effects during the peri-procedural phase of PCI in previous clinical and basic research; however, there is a lack of rigorous, randomized, and controlled studies. The aim of this study is to evaluate the efficacy and safety of SYD in decreasing PMI. Methods: This is a randomized, double-blind, placebo-controlled clinical trial. A total of 284 patients with unstable angina will be randomized into test and control groups. The two groups will be given SYD or a placebo (three times each day, four capsules each time) 3 days before PCI on the basis of conventional treatment. Twelve hours before PCI, an additional 4 capsules will be given, and drug treatment is planned to be maintained for 1 month after surgery. Dynamic changes in the myocardial enzyme in four time-points (before PCI, and 4, 24, 48 hours after PCI) in both groups of patients that will be observed. The follow-up period will be 1 month. The primary observation markers are planned to evaluate the efficacy and safety of SYD in decreasing PMI. The secondary observation markers will be to evaluate the major adverse cardiovascular events (MACEs) status at day 30 after PCI, (all-cause mortality, non-fatal myocardial infarction, repeated revascularization of target blood vessel) and Seattle Angina Questionnaire scores. GRACE scores will be used for risk stratification, and the intervention efficacy of SYD on PMI patients with different risks will be retrospectively evaluated. Discussion: This study will provide a rigorous clinical evidence to evaluate the efficacy and safety of SYD in decreasing PMI and the results are worth anticipating. Trial registration: The design of this trial has been registered with the Chinese Clinical Trial Registry (No. ChiCTR-IPR-17011069).

Aspirin is widely used in the treatment and prevention of coronary heart disease (CHD). It plays an important role in anti-platelet aggregation by inhibiting the activity of cyclooxygenase-1 (COX-1). On the other hand, the decrease of COX-1 activity inhibits the production of prostaglandin (PG) in gastric mucosa, which leads to the decrease of gastric mucosal blood flow and the weakening of mucous barrier. That makes the gastric mucosa more vulnerable to injury. We usually treat gastric mucous injury caused by long-term use of low-dose-aspirin (LDA) with drugs that inhibit gastric acid secretion. However, these drugs cannot improve gastric mucosal blood flow and the effect of gastric mucous barrier. And the long-term use of these drugs can lead to a variety of adverse reactions, such as dyspepsia, osteoporosis, nutritional deficiency and so on. This paper reviews the research progress of traditional Chinese medicine (TCM) in the treatment of gastric mucosa injury caused by LDA. It was found that Panax quinquefolius ( Xiyangshen ) saponins, Astragaloside A, Dendrobium officinale ( Tiepishihu ) polysaccharide, Bletilla Striata ( Baiji ), Jinghua Weikang capsule, Danhong injection and other TCM components or preparations can increase the level of PG in gastric mucosa and increase the blood flow of gastric mucosa, so as to improve the effect of gastric mucous barrier. This provides a certain idea for the prevention and treatment of gastric mucosa injury caused by long-term application of LDA in patients with CHD.

Lipid metabolism dysregulation plays a crucial role in the occurrence of atherosclerosis (As). SCAP/SREBP signaling is the main pathway for regulating lipid metabolism. Tetramethylpyrazine (TMP), a Traditional Chinese Medicine (TCM) for treating angina pectoris, has antiatherosclerotic effects and ameliorates blood lipids disturbance. However, its precise mechanism remains unclear. This study investigated the mechanism of TMP in ameliorating As in mice model. After six weeks of high-fat diet, 30 ApoE−/− mice were randomized (n = 10) and treated with Lipitor, TMP, or distilled water for six weeks. The serum blood lipids and insulin levels were measured. The expressions of PAQR3, Insig-1, SCAP, SREBP-1c, IRS-1, PI3K, Akt, and mTORC-1 in the adipose tissues were determined. The results showed that TMP could significantly decrease blood lipids levels, insulin, and corrected plaque area of the ApoE−/− mice as compared to the untreated mice (P < 0.05, P < 0.01). Moreover, TMP could significantly downregulate the expressions of SCAP, SREBP-1c, PAQR3, IRS-1, PI3K, Akt, and mTORC1 (P < 0.01). Thus, TMP may ameliorate lipid metabolism disorder and As by downregulating PAQR3 and inhibiting SCAP/SREBP-1c signaling pathway. In addition, PI3K/Akt/mTORC1 signaling pathway may be involved in this process.

Objectives. To survey and analyse the prognosis, outcome, and changing tendency of the Acute Myocardial Infarction (AMI) patients in Beijing third-grade A-level Traditional Chinese Medicine (TCM) hospitals.Methods. We collected the clinical datum of hospitalized AMI patients in Beijing 6 TCM hospitals from January 1999 to December 2008 and then analysed the clinical datum.Results. (1) The mean age of patients had showed a slowly rising tendency during this ten years. The patients who had previous history of cerebrovascular diseasea and multiple comorbidities had increased year by year. (2) The rate of reperfusion therapy, revascularization and standardized using of drug, and usage of TCM of AMI patients presented a significant increasing tendency in these hospitals. (3) The proportion of AMI patients combined with cardiac arrhythmia and heart failure had decreased significantly. (4) The AMI mortality presented a decreasing tendency in 10 years.Conclusions. The AMI patients in Beijing TCM hospitals had their own unique clinical features, and it can improve their prognosis by combined therapy of Western Medicine and Traditional Chinese Medicine.

Shen-Yuan-Dan Capsule (SYDC), a Chinese medicine used for treating angina pectoris, has anti-atherosclerotic effects in ApoE-deficient (ApoE-/-) mice. Autophagy and aberrant DNA methylation are indispensable in the pathogenesis of atherosclerosis. This study aimed to explore the methylation

Objectives.The study was to investigate the effects and mechanisms of Shen-Yuan-Dan (SYD) pharmacological postconditioning on myocardial ischemia/reperfusion (I/R) injury.Methods.In thein vivoexperiment, myocardial injury markers and histopathology staining were examined. In thein vitroexperiment, cell viability and cell apoptosis were, respectively, detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays and Hoechst 33342 fluorochrome staining. The protein expressions of Bcl-2 and Bax were determined by immunocytochemistry assay.Results.Both low and high doses of SYD protected myocardium against I/R injury in rat model by reducing lactic dehydrogenase (LDH) and creatine kinase-MB (CK-MB) activity and malondialdehyde (MDA) content, increasing superoxide dismutase (SOD) activity and attenuating histopathology injury. Meanwhile, in thein vitroexperiment, SYD promoted cell viability and inhibited the cardiomyocyte apoptosis. The level of Bcl-2 protein was restored to the normal level by SYD pharmacological postconditioning. In contrast, the Bax protein level was markedly reduced by SYD pharmacological postconditioning. These effects of SYD were inhibited by LY294002.Conclusions.The results of this study suggested that SYD pharmacological postconditioning has protective effects against myocardial I/R injury in bothin vivoandin vitromodels, which are related to activating the phosphatidylinositol 3-kinase/Akt (PI3K/Akt) pathway.

Lipid metabolism dysregulation plays a crucial role in the occurrence of atherosclerosis (As). SCAP/SREBP signaling is the main pathway for regulating lipid metabolism. Tetramethylpyrazine (TMP), a Traditional Chinese Medicine (TCM) for treating angina pectoris, has antiatherosclerotic effects and ameliorates blood lipids disturbance. However, its precise mechanism remains unclear. This study investigated the mechanism of TMP in ameliorating As in mice model. After six weeks of high-fat diet, 30 ApoE−/−mice were randomized (n=10) and treated with Lipitor, TMP, or distilled water for six weeks. The serum blood lipids and insulin levels were measured. The expressions of PAQR3, Insig-1, SCAP, SREBP-1c, IRS-1, PI3K, Akt, and mTORC-1 in the adipose tissues were determined. The results showed that TMP could significantly decrease blood lipids levels, insulin, and corrected plaque area of the ApoE−/−mice as compared to the untreated mice (P<0.05,P<0.01). Moreover, TMP could significantly downregulate the expressions of SCAP, SREBP-1c, PAQR3, IRS-1, PI3K, Akt, and mTORC1 (P<0.01). Thus, TMP may ameliorate lipid metabolism disorder and As by downregulating PAQR3 and inhibiting SCAP/SREBP-1c signaling pathway. In addition, PI3K/Akt/mTORC1 signaling pathway may be involved in this process.