Objective To investigate the relationship between regular exercise habit and coronary collaterals of patients with acute coronary syndrome (ACS).Methods TWo hundred and thirty-night patients diagnosed ACS and operated coronary angiography (CAG) showing severe coronary stenosis were enrolled hospitalized from May 2012 to October 2012.They were divided into regular exercise group (n =102) and irregular exercise group(n =137) according to the exercise frequency.The information of the general data,the information of CAG and other relevant index were collected.The coronary artery score was recorded according to the Censini and the coronary collateral class was made according to the Rentrop.Other characters in clinical and laboratory were recorded.Multi-factor regression analysis was used to analysis the influence factors of coronary collateral.Results The proportion of coronary collaterals (41.2％ (42/102)) in the regular exercise group was higher than that in the irregular exercise group (24.1％ (33/137)),and the difference was statistically significant(x2 =7.929,P =0.005).Lg(Gensini score) was (1.89 ± 0.18) the and (1.94 ± 0.19) in the regular exercise group,The left ventricular ejection fraction was 57.0％ (52.0％,60.0％) in the regular exercise group and 50.0％ (45.0％,57.0％) in the irregular exercise group,and the difference was statistically significant (Z =-5.152,P =0.000).Multi-factor regression analysis showed that regular exercise (OR =3.423,95％ CI:1.790-4.578),diabetes mellitus (OR =0.451,95％ CI:0.212-0.962),B-type natriuretic peptide (OR =2.412,95 ％ CI:1.271-4.578),non-ST-segment elevation ACS (OR =2.383,95％ CI:1.185-4.791),chest pain history (OR =2.207,95％ CI:1.175-4.145),Gensini score (OR =1.538,95％ CI:1.141-2.073) were independent influence factors of coronary collateral(P ＜ 0.05).After adjusting other factors,the patients with regular exercise had better coronary collaterals than that with irregular exercise (OR=3.423,95％CI:1.790-6.548,P ＜0.001).Conclusion The regular exercise can promote coronary collateral emergence for the patients with ACS.

ObjectiveTo investigate the effect of resveratrol on the expressions of E-selectin and monocyte chemoattractant protein-1 (MCP-1) in activated endothelial cells.Methods After being pretreated with resveratrol followed by tumor necrosis factor-α (TNF-α) stimulation, human umbilical vein endothelial cells (HUVEC) were randomly divided into three groups: TNF group,resveratrol+TNF-α group and control group. The expression of E-selectin molecule on the surface of HUVEC was detected by flow cytometric analysis and the mRNA expressions of E-selectin and MCP -1 were determined by semiquantitative RT-PCR. ResultsTNF-α induced the expression of E-selectin and MCP-I of HUVEC.Resveratrol (10 μmol/L) inhibited E-selectin expression.The positive cells of E-selectin in TNF group, resveratrol + TNF-α group and control group were(47.84±3.2)%, (15.3±1.7)% and (3.74±1.6)%, respectively, and the differences among the three groups were statistically significant (P<0.05). Conclusions Resveratrol may contribute to the anti-atherosclerotic effect by inhibiting the expression of E-seleetin and MCP-1 of HUVEC.

Objective To explore the effect of resveratrol on the expression of matrix metalloproteinases-9 (MMP-9) in soluble CD40 ligand (sCD40L)-activated macrophages. Methods Human monocytic cell line THP-1 cells under an inducing of phorbol ester differentiated into macrophages. Then the macrophages were sitimulated by sCD40L independently and after a preincubation with resveratrol. The mRNA expression of MMP-9 and tissue-inhibitor of metalloproteinase-1 (TIMP-1) in macrophages were investigated by semiquantitative RT-PCR. The secretions of MMP-9 and TIMP-1 protein were measured by Western blot. The MMP-9 activity was analyzed by gelatin zymography technique. Results The expressions of MMP-9 gene(1.53±0.04 vs. 0.75±0.01,P＜0.05) and protein(244 930.8±31 268.6 vs. 192 976.8±20 223.1,P＜0.05)were higher in macrophages when stimulated by sCD40L. Resveratrol (10 μmol/L and 50 μmol/L)can inhibit the CD40L-induced gene expression and the protein secretion of MMP-9 (P＜0.01). The activity of MMP-9 was degraded by resveratrol (P＜0.05). Meanwhile resveratrol could increase the gene expression and protein secretion of TIMP-1 (P＜0.05). Conclusions Resveratrol can inhibit the CD40L-activated macrophage expression of MMP-9. It may be one of its mechanisms on antiatherosclerosis and stabilization of atheromatous plaques.

Background Resveratrol has been unanimously recognized as an cardiovascular protective substance in red wine. It has been speculated that the anti-atherosclerosis effect of resveratrol is ascribed to its powerful anti-inflammatory effect. Objective To investigate the effects of resveratrol on injured human umbilical veno-endothelial cells (HUVEC) and the reactive oxygen species(ROS) production induced by TNF-? or soluble CD40L (sCD40L). Methods Cultured HUVEC were pre-incubated with resveratrol(1-50 ?mol/L) for 2 hours and then treated with TNF-?(10 ?g/L) or sCD40L?(10 ?g/L) for another 4 hours. MTT assay was used to detect proliterative activity of HUVEC. Immunofluorescence microscopy was used for determination of ROS expression. Results Both TNF-? and sCD40L impaired HUVEC proliferation (-32.7% and -26% vs control,P

OBJECTIVE： To systematically review the efficacy and safety of colesevelam hydrochloride combined with other hypoglycemic drugs in the treatment of T2DM， and to provide evidence-based reference for clinical treatment of T2DM. METHODS： Retrieved from PubMed， Embase， Medline， Cochrane Library， CJFD， VIP and Wanfang database during database establishement-Jul. 2019， randomized controlled trials （RCT） about the efficacy and safety of colesevelam hydrochloride combined with other hypoglycemic drugs （trial group） vs. placebo or other hypoglycemic drugs （control group） in the treatment of T2DM were collected. After extracting data from clinical studies that met the inclusion criteria， the quality of the studies was evaluated by Cochrane System Evaluator Manual 5.1.0. Meta-analysis was conducted by using Rev Man 5.3 statistical software in respects of the levels HbA1c， FPG， LDL-C， the incidence of total ADR， incidence of hypoglycemia and incidence of gastrointestinal ADR. RESULTS： A total of 11 RCTs were included， involving 2 625 patients. Results of Meta-analysis showed that HbA1c levels [MD＝－0.37， 95％CI（－0.51， －0.22），P＜0.001]， FPG level [MD＝－0.47， 95％CI（－0.88， －0.07）， P＝0.02] and LDL-C level [MD＝－0.38， 95％CI（－0.49， －0.28）， P＜0.001] in trial group were significantly lower than control group， with statistical significance. In terms of safety， the incidence of total ADR [OR＝1.24， 95％CI（1.06， 1.45）， P＝0.007] and gastrointestinal ADR [OR＝1.78，95％CI（1.05， 3.02），P＝0.03] in trial group were significantly higher than control group， with statistical significance. There was no significant difference in the incidence of hypoglycemia [OR＝1.03， 95％CI（0.62，1.72），P＝0.90]. CONCLUSIONS： Colesevelam hydrochloride combined with other hypoglycemic drugs can effectively reduce the levels of HbA1c， FPG and LDL-C in T2DM patients， but attention should be paid to the occurrence of gastrointestinal ADR.

Objective:To explore the interventional effect of β-sitosterol on ovalbumin(OVA)-induced allergic asthma rats and its potential mechanism.Methods:SD male rats were randomly divided into normal group(CON),model group(M),positive drug dexamethasone group(DEX,0.075 mg/kg)and β-sitosterol group(Sit,50 mg/kg).A rat model of allergic asthma was estab-lished by intraperitoneal injection of OVA with aluminum hydrogen solution,and nebulized inhalation of OVA to stimulate.Rats were given intragastric administration 30 min before aerosol challenge,and after continuous administration for 7 days,the indicators of cough and asthma and tracheal phenol red excretion were detected.HE staining was used to observe pathological changes of lung tis-sue.Flow cytometry was used to detect reactive oxygen species(ROS)generation,apoptosis level and ratios of Th17 and Treg cells in peripheral blood.Biochemical method was used to detect contents of MDA,and activities of T-SOD and GSH-Px in rat lung tissues.ELISA was used to detect levels of Th17 and Treg-related cytokines(TNF-α,IL-4,IL-6,IL-17A,and IL-35).Results:Compared with model group,β-sitosterol significantly prolonged the incubation period of cough and gasp in rats with allergic asthma,reduced the frequency of cough and gasping,and promoted the excretion of phenol red in trachea;significantly reduced inflammatory infiltration in lung tissue of asthmatic rats;observably reduced MDA content in lung tissue,ROS of primary lung cell and apoptosis levels of asthmatic rats,increased the activities of T-SOD and GSH-Px;markedly reduced proportion of Th17 cells and levels of pro-inflammatory cyto-kines TNF-α,IL-4,IL-6 and IL-17A,increased proportion of Treg cells and levels of anti-inflammatory cytokine IL-35.Conclusion:β-sitosterol can ameliorate airway inflammation and oxidative damage in OVA-induced allergic asthmatic rats,and its mecha-nism may be related to the regulation of β-sitosterol on Th17/Treg immune imbalance and oxidative stress response.

ObjectiveTo explore the mechanism of Xianglian Huazhuo prescription in the treatment of chronic atrophic gastritis （CAG） based on network pharmacology and animal experiments，so as to provide scientific basis for clinical application. MethodThe possible targets and pathways of Xianglian Huazhuo prescription in the treatment of CAG were obtained based on the prediction of network pharmacology. The CAG rat model was induced by sodium salicylate，N-methyl-N'-nitro-N-nitrosoguanidine （MNNG） and hunger and satiety disorder. Then the CAG rats were treated with Xianglian Huazhuo prescription and morodan for 60 days. After administration，the rats were sacrificed，and the content of interleukin-6 （IL-6），tumor necrosis factor-α （TNF-α），interleukin-1β （IL-1β） and vascular endothelial growth factor （VEGF） in serum was determined by enzyme linked immunosorbent assay（ELISA）. In addition， the protein expression of Bad and Bcl-2 in gastric mucosa was detected by immunohistochemistry （IHC）. ResultA total of 241 active components of Xianglian Huazhuo prescription and 53 core targets were obtained. Xianglian Huazhuo prescription affected multiple biological processes，such as cell proliferation and apoptosis，inflammatory reaction，regulation of DNA metabolism，and cell response to redox，as well as phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt），TNF，mitogen-activated protein kinase （MAPK），cancer and cancer-related signaling pathways. The animal model verification showed that Xianglian Huazhuo prescription lowered the levels of IL-6，TNF-α，IL-1β and VEGF in serum of CAG rats，and reduced the protein expression of Bad and Bcl-2 in gastric tissue. ConclusionXianglian Huazhuo prescription could regulate PI3K/Akt signal pathway and improve gastric mucosal injury in CAG by participating in biological processes such as cell proliferation，apoptosis and inflammation.

ObjectiveTo investigate the therapeutic effect and mechanism of coptisine on chronic atrophic gastritis （CAG） in rats based on the phosphatidylinositol 3-kinase （PI3K）/protein kinase B （Akt）/mammalian target of rapamycin （mTOR） signaling pathway. MethodA CAG rat model was induced by multiple factors， including sodium salicylate， N-methyl-N′-nitro-N-nitrosoguanidine （MNNG）， and irregular feeding. The successfully modeled rats were randomly divided into the model group， folic acid group， and high- and low-dose coptisine groups. The high- and low-dose coptisine groups were given coptisine （50， 10 mg·kg^-1， respectively）， and the folic acid group was given folic acid at 2 mg·kg^-1 for 60 days. The pathological changes were detected by hematoxylin-eosin （HE） staining. The ultrastructure of gastric mucosal cells was observed by electron microscopy. Serum pepsinogen Ⅰ （PGⅠ）， pepsinogen Ⅱ （PGⅡ）， and PGⅠ/PGⅡ ratio （PGR） were detected by immunoturbidimetry. Serum gastrin-17 （G-17） level was detected by radioimmunoassay. The content of interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β） in serum of rats was detected by enzyme-linked immunosorbent assay （ELSIA）. Western blot analysis was used to detect the expression levels of TGF-β₁， PI3K， phosphorylated-Akt （p-Akt）， mTOR， and phosphatase and tensin homolog deleted on chromosome 10 （PTEN） in gastric mucosa. The mRNA levels of TGF-β₁， PI3K， Akt， mTOR， PTEN， microtubule-associated protein light chain 3Ⅱ （LC3Ⅱ）， and Beclin-1 were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultCompared with the normal group， the model group showed atrophy and reduced number of intrinsic glands in the gastric mucosal tissues， as well as inflammatory cell infiltration. The ultrastructure of gastric mucosal cells in the model group displayed nuclear condensation， reduced and swollen mitochondria， and abnormal structure. The serum levels of G-17， PGⅠ， PGR， and the protein and mRNA levels of PTEN in gastric tissues were significantly lower in the model group （P<0.01）， while serum levels of IL-6， IL-1β， TNF-α， and the protein and mRNA levels of TGF-β₁， PI3K， Akt， and mTOR in gastric tissues were significantly higher （P<0.01）. Compared with the model group， various drug intervention groups showed different degrees of improvement in pathological damage and gastric mucosal cell ultrastructure， significantly increased serum levels of G-17， PGⅠ， and PGR （P<0.05，P<0.01）， and significantly decreased levels of IL-6， IL-1β， and TNF-α （P<0.05，P<0.01）. The high-dose coptisine group significantly downregulated the protein and mRNA levels of TGF-β₁， PI3K， Akt， and mTOR （P<0.05，P<0.01）. ConclusionBerberine has a therapeutic effect on CAG in rats， possibly exerting a protective effect on gastric mucosa by inhibiting inflammation and blocking the PI3K/Akt/mTOR signaling pathway.