Abstract:Aim To investigate the effect of microRNA-223 (miR-223) on apoptosis and oxidative stress of human adipose tissue-derived mesenchymal stem cell (hADSC) induced by advanced glycosylation end product (AGE). Methods The hADSCs were isolated and cultured by enzymatic digestion, and flow cytometry was used to detect the surface antigen (CD14, CD34, CD45, CD90, CD105 and HLA-DR) of hADSC. The hADSCs were divided into 6 groups:bovine serum albumin (BSA) group, AGE modified BSA (AGE-BSA) treatment group, miR-223 mimic transfection group, miR-223 mimic transfection＋AGE-BSA group, miR-223 inhibitor transfection group, and miR-223 inhibitor transfection＋AGE-BSA group. Cell viability and apoptosis rate were evaluated by CCK-8 assay and TUNEL assay respectively.Western blot was used to assess the expression of Cleaved Caspase3 protein in hADSC. The content of reactive oxygen species (ROS) in hADSC was determined by 2’,7’-dichlorfluorescein-diacetate (DCFH-DA) reagent kit. Results The hADSCs were positive for stem cell markers, including CD14, CD90 and CD105, and negative for CD34, CD45 and HLA-DR, as shown by flow cytometry. CCK-8 method, TUNEL staining, Western blot and DCFH-DA test results showed that:Compared with the BSA control group, the hADSC apoptosis rate, miR-223 expression, Cleaved Caspase3 protein expression and ROS production increased significantly in AGE-BSA treatment group, but hADSC survival rate decreased (P＜0.05); Compared with AGE-BSA treatment group, miR-223 mimic transfection could further increase the hADSC apoptosis rate, Cleaved Caspase3 protein expression and ROS production induced by AGE-BSA, and could further reduce hADSC survival rate (P＜0.05); Compared with AGE-BSA treatment group, miR-223 inhibitor transfection could inhibit the increases of hADSC apoptosis rate, Cleaved Caspase3 protein expression and ROS production, and could prevent the decrease of hADSC survival rate induced by AGE-BSA (P＜0.05). Conclusion High expression of miR-223 can promote the hADSC apoptosis and ROS production, and miR-223 may serve as a new target for the regulation of hADSC in promoting the healing of diabetic wound.

Abstract:Aim To investigate whether CD137-CD137L signal through tumor necrosis factor receptor-associated factor-6/c-Jun amino-terminal kinase/activated protein-1 (TRAF6/JNK/AP-1) pathway to regulate the expression of nuclear factor of activated T cell c1 (NFATc1) in mouse vascular smooth muscle cell (VSMC). Methods Mouse primary VSMCs were cultured from aortic tissue block, and third to fifth generations of cells were used for the experiment. VSMCs were divided into 6 groups:control group, CD137 stimulation group, CD137 inhibition group, siTRAF6 intervention group, siJNK intervention group and siAP-1 intervention group. The expression levels of TRAF6, phosphorylated JNK (p-JNK), phosphorylated AP-1 (p-AP-1) and NFATc1 protein were detected by Western blot in each group. The fluorescence expression of TRAF6, p-JNK, p-AP-1 and NFATc1 were detected by immunofluorescence assay in each group. Results (1)Compared with control group, the expression levels of TRAF6, p-JNK, p-AP-1 and NFATc1 protein were significantly increased in CD137 stimulation group (CD137-CD137L signal activation) (P＜0.05). Compared with CD137 stimulation group, the expression levels of TRAF6, p-JNK, p-AP-1 and NFATc1 protein were significantly decreased in CD137 inhibition group (CD137-CD137L signal inhibition) (P＜0.05). (2)The siRNA technology was used to silence TRAF6, JNK and AP-1 respectively. Compared with CD137 stimulation group, the expressions of TRAF6, p-JNK, p-AP-1 and NFATc1 were significantly reduced in siTRAF6 intervention group (P＜0.05); The expression of TRAF6 had no change, while the expression of p-JNK, p-AP-1 and NFATc1 were significantly decreased in siJNK intervention group (P＜0.05); The expressions of TRAF6 and p-JNK had no significant change, while the expressions of p-AP-1 and NFATc1 were significantly decreased in siAP-1 intervention group (P＜0.05). (3)Immunofluorescence assay showed that the fluorescent expressions of TRAF6, p-JNK, p-AP-1 and NFATc1 were increased in CD137 stimulation group (P＜0.05), and the fluorescent expressions of TRAF6, p-JNK, p-AP-1 and NFATc1 were significantly decreased in CD137 inhibition group (P＜0.05). The fluorescent expressions of TRAF6, p-JNK, p-AP-1 and NFATc1 were consistent with the above protein expressions in siTRAF6 intervention group, siJNK intervention group and siAP-1 intervention group. Conclusion CD137-CD137L signal can affect the expression of NFATc1 through the TRAF6/JNK/AP-1 pathway.

Abstract:Aim To explore the effects of epigallocatechin gallate (EGCG) on the inflammation of vascular endothelium in hyperuricemia rats. Methods Thirty-six male SD rats were divided into normal control group, model control group, EGCG low dose (EGCG-L) group, EGCG medium dose (EGCG-M) group, EGCG high dose (EGCG-H) group and allopurinol group. After five weeks, the expression of MCP-1, TNF-α, ICAM-1, ET-1 and eNOS in hyperuricemia rats were detected by RT-PCR, serum uric acid, creatinine, urea nitrogen and xanthine oxidase (XO) were determined. Results Compared with normal control group, the levels of serum uric acid and XO were increased in model control group (P＜0.01). Compared with model control group, the levels of serum uric acid and XO were significantly decreased in EGCG-L group, EGCG-M group, EGCG-H group and allopurinol group (P＜0.01). Compred with normal control group, the mRNA expression of MCP-1, TNF-α and ICAM-1 was markedly increased in model control group (P＜0.01). The expression of MCP-1 mRNA in EGCG-H group and allopurinol group was markedly decreased as compared with model control group (P<0.05). Compared with model control group, the expression of TNF-α, ICAM-1 mRNA was significantly decreased in EGCG-L group, EGCG-M group, EGCG-H group and allopurinol group (P＜0.01). The mRNA expression of ET-1 in EGCG-M group was also decreased significantly (P＜0.01). Conclusion EGCG attenuated serum uric acid and the inflammation of vascular endothelium in hyperuricemia rats.

Abstract:Aim To investigate the effect of extracellular superoxide dismutase (EC-SOD) on oxidative stress induced by homocysteine (Hcy) in macrophages and its mechanism. Methods THP-1 monocyte was stimulated by phorbol ester for 48 hours and evolved into macrophages. The macrophages were dealt with 0,0, 0,0, 500 μmol/L Hcy for 72 hours, and adding a folate acid＋vitamin B12 (VitB12) intervention group (100 μmol/L Hcy＋30 μmol/L folate acid＋30 μmol/L VitB12). The changes of oxidative stress indexes (H₂O₂, O₂－, OH－) were detected by microplate test.The mRNA expression of EC-SOD was detected by real-time fluorescence quantitative PCR and the protein expression of EC-SOD was detected by Western blot in macrophages. EC-SOD assay kit was used for detecting EC-SOD activity. EC-SOD recombinant plasmid and interfering plasmid were constructed and transfected into cells, and expressions of EC-SOD mRNA, protein and superoxide anion were detected in macrophages. Results Compared with the control group, H₂O₂ and OH－ activities were significantly increased, and EC-SOD mRNA and protein expressions were significantly decreased in 0,0, 500 μmol/L Hcy group (P＜0.01). Compared with the control group, the EC-SOD activity was respectively decreased by 13.92%, 8.62%, 10.32% in 0,0, 500 μmol/L Hcy group (P＜0.05 or P＜0.01). Compared with the 100 μmol/L Hcy group, the expression of EC-SOD mRNA was increased by 47% in folate acid＋VitB12 intervention group.After transfection of EC-SOD recombinant plasmid and interfering plasmid, compared with the 100 μmol/L Hcy group, O₂－ content was decreased by 63.89% in EC-SOD recombinant group, while O₂－ content was increased by 33.59% in interfering fragment -596 group (P＜0.05 or P＜0.01). Conclusions EC-SOD is involved in the oxidative stress induced by Hcy in monocyte-derived macrophages. EC-SOD may play an important role in the inhibition of atherosclerosis induced by Hcy.

Abstract:Aim Trying to establish a lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) bicistronic gene expression vector and detect its expression and function in 293T cell, to explore the role of LOX-1 in atherosclerosis and lay a foundation for establishing intervention mechanism of LOX-1 targets. Methods First human LOX-1 gene was obtained from human cDNA by PCR and cloned into T plasmid. After sequencing, recombinant T plasmid was subcloned into bicistronic eukaryotic expression plasmid pIRES2 AcGFP1-Nuc. Next the bicistronic recombinant expression plasmid was transfected into 293T cells by liposome. Plasmid transfection efficiency was detected by inverted fluorescence microscope. Then the expression of exogenous human LOX-1 gene and protein in 293T cells was detected by RT-PCR and Western blot. The expression of human LOX-1 in 293T cells membrane was detected by confocal laser. Finally LOX-1 functions of binding with ox-LDL in 293T cell membrane was detected by confocal laser and flow cytometry. Results The pIRES2-LOX-1 bicistronic recombinant plasmid was constructed successfully. After transfection, green fluorescent protein was detected and the abundant LOX-1 mRNA and protein were expressed in the transfected cells, moreover human LOX-1 were expressed in the 293T cells membrane and could bind with ox-LDL. Conclusion We have successfully established a LOX-1 gene bicistronic expression vector and on the basis we testified human LOX-1 expressed in 293T cells membrane and could bind with ox-LDL, which layed a foundation for further study of its effect in atherosclerosis and establishing intervention mechanism of LOX-1 targets.

Abstract:Aim To explore the role and mechanism of different concentrations of resveratrol in the neurological function and the expression of tumor necrosis factor-α (TNF-α) of cerebrally injured rats with ischemia-reperfusion. Methods The 150 healthy adult male SD rats were randomly divided into 5 groups:sham operation group, model group, low dose resveratrol (2.5 mg/kg) group, middle dose resveratrol (5 mg/kg) group, high dose resveratrol (10 mg/kg) group, 30 rats for each group. Model group and resveratrol group were given with normal saline or different concentrations of resveratrol by intraperitoneal injection 20 minutes before the reperfusion. The nerve function defect scores were evaluated 6 hours, 24 hours, 48 hours, 72 hours, and 7 days of time after the operation. The cerebral infarction focus volume was calculated and the difference among the five groups was compared after TTC staining of brain tissues; the TNF-α was tested around the area of ischemia brain tissues by immunohistochemistry, and the differences was compared among the five groups. Results (1) Comparison of neurological deficit scores:the intervention of different concentrations of resveratrol has significantly improved the neurological deficit of rats, meanwhile, the higher the dose of resveratrol was, the more obvious the improvement of rats' neurological deficit has got, and it was in a dose-dependent manner. (2) Comparison of cerebral infarction focus volumes:the intervention of different concentrations of resveratrol has significantly reduced the cerebral infarction volumes of rats in different groups (P<0.05), and the higher the dose of resveratrol was, the larger the volume of reduced cerebral infarction was, and it was in a dose-dependent manner. (3) Comparison of immunohistochemistry of tissues surrounding the cerebral ischemia areas:at different hours, the numbers of TNF-α positive cells in the brain tissues surrounding the rats' cerebral ischemia area were:model group> low dose resveratrol group> middle dose resveratrol group> high dose resveratrol group> sham operation group (P<0.05), and the higher the dose of resveratrol was, the smaller the number of TNF-α positive cells were (P<0.05), which was in a dose-dependent manner. Conclusions (1) In the process of cerebral ischemia-reperfusion injury, resveratrol can reduce cerebral infarction volume and improve neurological deficit scores in a dose-dependent manner. It can also inhibit the expression of TNF-α through some kind of mechanism. (2) The protective effects of resveratrol on cerebral ischemia reperfusion injury was dose-related, and showed a significant dose-dependent manner.

Abstract:Aim To observe the effect of putative receptor protein related to the angiotensin receptor AT1 (APJ) agonist Apelin-13 on the hypertensive renal fibrosis and to explore the possible mechanism in spontaneously hypertensive rat (SHR). Methods Male SHRs of 12 weeks old were randomly divided into control group and 1 μg/(kg·d) Apelin-13 group, 10 μg/(kg·d) Apelin-13 group, 100 μg/(kg·d) Apelin-13 group. The rats were administrated with Apelin-13 by tail vein for 12 weeks. 24 h urine protein was continuously measured. Serum creatinine and urea nitrogen were measured. Systolic blood pressure (SBP) was continuously measured by tail method. Histological change of kidney was observed by HE staining and Masson staining. The expressions of autophagy related protein microtubule-associated protein light chain-3 (LC3), Beclin-1 and the autophagy substrates p62 in the kidney were determined by Western blot. Results Compared with control group, SBP, 24 h urine protein, serum creatinine and urea nitrogen, renal injury score and collagen volume fraction were significantly decreased in dose-dependent manner in 10 μg/(kg·d) Apelin-13 group and 100 μg/(kg·d) Apelin-13 group (all P<0.05). The edema of renal tubular epithelial cells was alleviated, the interstitial collagen deposition was decreased, and the degree of renal interstitial fibrosis was decreased in 10 μg/(kg·d) Apelin-13 group and 100 μg/(kg·d) Apelin-13 group. Compared with control group, LC3-Ⅱ expression, LC3-Ⅱ/LC3-Ⅰ ratio and Beclin-1 expression were singificantly increased and p62 expression was singificantly decreased in kidney in dose-dependent manner in 10 μg/(kg·d) Apelin-13 group and 100 μg/(kg·d) Apelin-13 group (all P<0.05). Conclusion Apelin-13 inhibits the progression of hypertensive renal fibrosis, and its mechanism may be related to the inhibition of autophagy by Apelin-13.

Abstract:Aim To examine myocardial bridge-mural coronary artery (MB-MCA) by using coronary CT angiography (CTA) and coronary angiography (CAG); To investigate the clinical features of MB-MCA and correlation between its imaging indexes and myocardial ischemic symptoms. Methods MB cases were retrospectively analyzed in our hospital in recent years, and 152 cases of MB were selected and diagnosed by coronary CTA and CAG. According to whether there was atherosclerosis (As), 152 cases of MB were divided into simple MB group and As with MB group. According to whether there was myocardial ischemic symptom, 152 cases of MB were divided into symptomatic group and asymptomatic group. Clinical features and imaging data were analyzed and compared in each group. Correlation was analyzed between MB-MCA imaging indexes and myocardial ischemia symptoms. Results The detection rate of coronary artery CTA for MB was 11.4%, and the detection rate of CAG for MB was 10.1%, and both were close. MB-MCA features of 152 cases:Systolic compression degree was 50.1%±10.5%, diastolic compression degree was 22.8%±10.5%; The average length was 18.2±11.5 mm mm, and the thickness was 2.7±0.8 mm; The most common MB site was in the middle part of left anterior descending coronary artery (LAD) (60.7%). Incidence of myocardial ischemic symptoms (typical chest tightness, etc.) and positive rate of treadmill exercise test in As with MB group were significantly higher than those in simple MB group (75.5% vs 58.7%, 66.0% vs 43.5%, P＜0.001). Compared with the asymptomatic group, MB was more distributed in the middle part of LAD, and more easily complicated with As in the symptomatic group (86.9% vs 68.9%, 74.8% vs 57.8%, P＜0.001). Spearman correlation analysis showed that the MB thickness, MCA systolic and diastolic compression degree were positively correlated with the myocardial ischemic symptoms. Conclusions The detection rates of coronary CTA and CAG for MB are similar. Incidence of myocardial ischemic symptoms and positive rate of treadmill exercise test in patients with MB combined with As are higher than those in patients with simple MB. Myocardial ischemic symptoms in patients with MB are closely related to MB thickness, MCA compression degree and As.

Abstract:Aim To investigate the correlation between insulin resistance (IR) and degree of coronary artery lesion in patients with coronary heart disease (CHD) and impaired glucose tolerance (IGT). Methods 152 CHD patients with IGT, and 35 CHD patients with non-IGT (control group) were enrolled in this study. IR index (HOMA2-IR) was determined by HOMA2 method. Gensini score system was used to assess the degree of coronary artery stenosis quantitatively, and the type B₂/C lesions were defined as complex lesions of the coronary artery. Taking the HOMA2-IR quartile as the cutoff point, 152 CHD patients with IGT were divided into 4 groups:the first quartile group (n＝38), the second quartile group (n＝38), the third quartile group (n＝38), the fourth quartile group (n＝38). Baseline data and the results of coronary angiography were compared among the five groups. Results 2 hour postprandial blood glucose (2hPBG), glycosylated hemoglobin A1 (HbA1c), fasting insulin and Gensini score increased gradually in the 5 groups, the difference was statistically significant (P＜0.01). Coronary multiple lesions and B₂/C lesions in fourth quartile group were significantly higher than those in first quartile group and control group (P＜0.05). Correlation analysis showed that Gensini score was positively correlated with HOMA2-IR (r＝0.712, P＜0.001). Multivariable stepwise regression analysis showed that HOMA2-IR, HbA1c and 2hPBG were the independent risk factors affecting the degree of coronary artery stenosis. Logistic regression analysis showed that HOMA2-IR was an independent risk factor for multiple lesions and B₂/C lesions. Conclusion IR is an important index reflecting the degree of coronary artery stenosis in patients with CHD and IGT.

Abstract:Aim To investigate the correlation of epicardial adipose tissue (EAT), serum ischemia modified albumin (IMA) and high-sensitivity cardiac troponin T (hs-cTnT) in patients with acute coronary syndrome (ACS). Methods 120 cases of ACS in our hospital from September 2014 to November 2015 were selected as the case group, including 40 cases in single vessel disease group, double vessel disease group and multiple vessel disease group. 120 cases with normal healthy cardiac function in our hospital physical examination were selected as the control group. EAT thickness was measured by echocardiography, IMA was measured by albumin cobalt ion combined with serum test, serum hs-cTnT levels were measured by electro chemiluminescence immunoassay. Results EAT thickness, IMA and hs-cTnT levels and Gensini scores in ACS patients were significantly higher than those in normal control group (P＜0.01). In ACS patients, the EAT thickness, IMA, hs-cTnT and Gensini score in single vessel disease group, double vessel disease group and multiple vessel disease group were all increased, and were higher than those in control group (P＜0.01). EAT thickness, IMA and hs-cTnT levels were significantly positively correlated with Gensini score (P＜0.01) in patients with ACS. IMA level of single vessel lesion group was correlated with Gensini score (P＜0.05), EAT thickness and hs-cTnT level had no significant correlation with Gensini score (P＞0.05). EAT thickness, IMA and hs-cTnT level were significantly positively correlated with Gensini score in double vessel group and multiple vessel disease group (P＜0.05 or P＜0.01). Conclusion EAT thickness, IMA and hs-cTnT levels were correlated with the severity of ACS lesions.

Abstract:Aim To investigate the predictive value of platelet to lymphocyte ratio (PLR) in myocardial reperfusion blood flow and major adverse cardiac and cerebrovascular events (MACCE) in patients with acute ST-segment elevation myocardial infarction (STEMI). Methods Clinical and angiographic data of 181 patients with STEMI who received direct PCI in our hospital during the period of hospitalization were retrospectively analyzed. According to the ROC curve to determine the diagnosis of no reflow in the PLR standard, the selected patients were divided into high PLR group and low PLR group, and the clinical data, incidence of MACCE during hospitalization period and follow-up in the two groups were compared. Results ROC curve analyzed the relationship between preoperative PLR and postoperative TIMI blood flow, and PLR≥162.72 predicted intraoperative no-reflow with a specificity of 85.5% and a sensitivity of 84.62%(AUC＝0.5,5%CI was 0.776～0.883, Z＝6.611, P＜0.001). All patients were divided into two groups including high PLR group (PLR≥162.72, n＝48) and lower PLR group (PLR＜162.72, n＝133), there were no significant differences in clinical data between the two groups. Compared with patients in low PLR group, patients in high PLR group had higher peak levels of creatine kinase-MB (313.55 ± 212.76 U/L vs. 216.64 ±152.41 U/L, P＝0.001), lower left ventricular ejection fraction (48.58%±7.30% vs. 51.66%±6.82%, P＝0.009), and higher incidence of MACCE in-hospital (20.83% (10/48) vs. 9.77% (13/133), P＝0.049). During a mean follow-up of 6~72 (25.57±18.72) months, a total of MACCE occurred in 28 cases, including 10 cases died from different reasons. The incidence of MACCE in high PLR group was significantly higher than that in low PLR group (27.08% (13/48) vs. 11.28% (15/133), P＝0.009). Survival analysis showed that the all-cause mortality and the events free survival in high PLR group was significantly higher than that in low PLR group (P＝0.003). COX proportional hazard regression analysis showed that high PLR was an independent risk factor for MACCE after myocardial infarction (HR＝2.6,5%CI＝1.794, P＝0.035). Conclusion PLR is an independent and valuable index for predicting the occurrence of MACCE after direct PCI in patients with STEMI.

Abstract:Aim To explore the relationship between cumulative heart rate exposure (cumHR) and brachial-ankle pulse wave velocity (baPWV). Methods A total of 7904 participants were selected from Kailuan Study stroke cohort and elderly population cohort to compose observation population, and finally 5153 cases were included in the study cohort. According to cumHR, the research subjects were divided into four groups. The correlation between cumHR and baPWV was analyzed by partial correlation analysis. The effects of cumHR on baPWV were analyzed by multivariate linear regression and multivariate Logistic regression. Results With the increase of cumHR, the average level of baPWV and the detection rate of baPWV≥1400 cm/s were on the rise. The results of partial correlation analysis showed that cumHR was positively correlated with baPWV (r＝0.35, P＜0.05), and after adjusting age and sex, cumHR was still positively correlated with baPWV (r＝0.24, P＜0.05). Multivariate linear regression analysis showed that cumHR increased by 1 beat/minute, baPWV increased 1.071 cm/s. Logistic regression analysis showed that after correction of other confounding factors, compared with the cumHR first group, cumHR second group, third group and fourth group were risk factors for baPWV≥1400 cm/s, and OR values (95%CI) were respectively 1.432 (1.121-1.829), 1.738 (1.371-2.204) and 2.475 (1.949-3.143). Conclusions cumHR is positively correlated with baPWV. cumHR is a risk factor for the increase of pulse wave velocity.

Abstract:Aim To investigate the effectiveness of the same and different drug-eluting stent in the treatment of coronary drug-eluting stent restenosis. Methods PubMed, OVID, Embase, Cochrane Library, Wanfang Database, China Journal Full-text Database(CNKI), Chinese Biomedical Literature Database (CBM), VIP Database (VIP) were retrieved. The materials of the treatment in coronary drug-eluting stent restenosis with the same and different drug-eluting stent were collected,10 studies were withdrawed, including 1680 patients. The RevMan5.2 analysis software was used in systematic review. Control test database computer retrieval to 2015 October. Results The different drug-eluting stent treatment in coronary drug-eluting stent restenosis was found to reduce the odds of target lesion revascularization (OR＝0.3,5%CI was 0.55~0.96, P＝0.02) and major adverse cardiovascular events (OR＝0.2,5%CI was 0.54~0.96, P＝0.03). There was no difference between the two groups in rates of death (OR＝1.3,5%CI was 0.49~2.16, P＝0.95) or myocardial infarction (OR＝0.9,5%CI was 0.24~1.41, P＝0.23). Conclusion For patients with restenosis after drug-eluting stent implantation, different drug-eluting stents are more benefit than the same drug-eluting stent implantation.

Abstract:Aim To establish a novel rat model of atherosclerosis. Methods 16 ApoE deficient rats(ApoE－/－ Rats) were divided into experimental group and control group on the average,and fed with high fat diet for 12 weeks. The experimental group received Alzet osmotic pump implanted subcutaneously in the first 4 weeks, filled with angiotensinⅡ(AngⅡ) , at a rate of 1 μg/(kg·min) uniform release,while the control group was only treated with equivalent saline. At the end of the twelfth week, the experimental animals were tested for body weight and blood collected. The inflammatory factors (interleukin-1β (IL-1β), tumor necrosis factor alpha (TNF-α)) and blood lipids (total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC)) were detected. Sacrificed after anesthesia, the heart and aortic full length were harvested for HE, oil-red-O and Masson staining. Results The atherosclerotic plaque was found in the experimental group, while the control group had no similar performance. There was no statistical difference between the two groups in other aspects. ConclusionApoE deficient rats could be induced atherosclerosis plaque successfully, when were treated with high fat diet and AngⅡ.

Abstract:Histamine is a biogenic amine involved in various pathophysiological processes, such as regulation of immune responses and anaphylactic reaction, neural signal transduction, secretion of gastric acid and hematopoiesis. The effects of histamine is dependent on its binding 4 subtypes of histamine receptors (HR), activating different intracellular pathways. Inflammation and immune responses play an important role in multiple cardiovascular disease, including coronary artery diseases, heart failure, myocarditis and pericarditis. The complex regulatory interaction between histamine and immune responses are receiving more and more attention. In this review, we will discuss the effects of histamine in innate immune responses and cardiovascular diseases.

Abstract:Early epidemiological studies have found that lower level of high density lipoprotein cholesterol (HDLC) is closely associated with an increased risk of coronary heart disease. This prompts a high density lipoprotein anti-atherosclerosis hypothesis:compared to low density lipoprotein cholesterol, HDLC is “good” cholesterol, and increased serum HDLC level may reduce the risk of cardiovascular events. However, new studies have found that elevated HDLC level does not reduce the occurrence of cardiovascular events. This makes the high density lipoprotein anti-atherosclerosis hypothesis be questioned. Recently, the relationship between high density lipoprotein function rather than HDLC level and atherosclerosis has been paid more attention. Latest related research of high density lipoprotein is described in this paper.

Abstract:Fibroblast growth factor 21 (FGF21) is a newly discovered metabolic regulatory factor in recent years. The relationship between FGF21 and diabetic macroangiopathy has become a research hotspot in recent years. The level of endogenous FGF21 is increased in patients with impaired glucose tolerance, and its level is progressively increased with the appearance of type 2 diabetes mellitus with macroangiopathy. It is speculated that the possible mechanism is FGF21 resistance. FGF21 gene is expressed in vascular endothelial cells, and FGF21 may play a protective role in the early stage of atherosclerosis, suggesting that FGF21 is expected to become a target for prevention and treatment of diabetic macroangiopathy.

Abstract:Buyanghuanwu decoction is a traditional formula which has good efficiency on the prevention and treatment of atherosclerosis, but its mechanism is still obscure. This paper summarized the Buyanghuanwu decoction’s mechanism on signaling pathway of aththerosclerosis including inflammatory pathway, Rho/Rho kinase signaling pathway, Toll like receptor signaling pathway, matrix metalloproteinases signaling pathway and so on.