Objective To assess the effects of Guanxinshutong capsule(GXST)on protection of left ventricular(LV)function after acute myocardial infarction(AMI)in rats.Methods Twenty-eight male Sprague Dawley rats were randomized to Model group,Drug group and Sham-operated group,with acute myocardial infarction(AMI)achieved by ligating coronary artery in Model and Drug groups.From one week before surgery to four weeks after surgery,GXST for Drug group(1.5 g/kg,2 times/day)or saline for Model and Sham-operated groups was administered via direct gastric gavage.After four weeks of treatment following surgery,measurement of LV function,pathohistological observation and analysis were performed.Results Compared with rats in the Model group,LV systolic pressure(LVSP)[(97.7 ± 9.0)mm Hg (1 mm Hg =0.133 kPa)vs(85.9 ±9.4)mm Hg],the maximum rising rate of LV pressure(+ dp/dtmax)[(4810.2 ± 595.0)mm Hg/s vs(3786.2 ± 723.0)mm Hg/s]and the maximum dropping rate of LV pressure(-dp/dtmax)[(3781.6 ±573.6)mm Hg/s vs(2774.4 ±633.5)mm Hg/s]in the Drug group were significantly increased,while LV end-diastolic pressure(LVEDP)[(10.3 ± 0.7)mm Hg vs(12.7 ±2.4)mm Hg]in the Drug group was significantly decreased(all P ＜ 0.05).Myocardial pathohistological morphology was improved in the Drug group with fibrosis alleviated[(5.13 ± 1.37)％ vs(7.27 ±1.01)％]and infarct size reduced[(20.14 ± 8.49)％ vs(31.90 ± 4.98)％].Apoptosis index(AI)was decreased[(14.05 ± 4.04)％ vs(20.87 ± 6.03)％]and vessel density was significantly increased by 1.48-fold in the Drug group(all P ＜ 0.05).Conclusions GXST is effective in protecting LV function after AMI in rats,which may be affect through increasing vessel density of infarction area,improving myocardial pathohistological morphology,alleviating fibrosis,reducing infarct size and decreasing AI.

Objective To expose the effect and its potential mechanism of vinpocetine (Vinp) on the restenosis of dia?betic grafted veins. Methods Thirty-six Sprague-Dawley rats were randomized into saline control group and Vinp treat?ment group. The autologous jugular vein to carotid artery transplantation was performed in diabetic model rats. Normal sa?line or Vinp were intraperitoneally injected. The rats were sacrificed at 0, 2 or 4 weeks after surgery, then the grafted veins were harvested. The pathological sections were used to detect the effect of Vinp on intimal hyperplasia. The protein expres?sion of proliferating cell nuclear antigen (PCNA) was detected by immunohistochemical method, and which was described by cell proliferation index. The phosphorylation of NF-κB was detected by Western blot assay. Results The treatment of Vinp on intimal hyperplasia in vivo was significant at two weeks after surgery (17.06±5.10)μm versus control group (39.79±7.84μm, P<0.01), (30.94±5.18)μm versus (63.67±18.09)μm at four weeks after surgery (P<0.01). Vinp treatment effectively reduced the protein expression of PCNA [2 weeks:(21.07±1.38)%vs. (28.13±1.35)%,P<0.01;4 weeks:(31.73±1.38)%vs. (63.67 ± 18.09)%, P<0.01]. The treatment of Vinp inhibited phosphorylation of NF-κB at two weeks (1.08 ± 0.42 vs. 0.84 ± 0.12, P < 0.01). Conclusion Vinpocetine can effectively attenuate intimal hyperplasia in diabetic grafted veins, which might be related to its effect on inhibiting phosphorylation of NF-κB as well as inflammation.

Background The protective effects against reperfusion injury of cardioprotective drugs have recently been evaluated and found to be inadequate. Guanxinshutong (GXST), a combination of the traditional herb and Mongolian medicine, is effective and safe in treating angina pectoris in clinical trials. We assess the cardioprotective effects of GXST against myocardial ischemia and reperfusion (MI/R) injury in rats and explore its possible mechanism. Methods Forty-five male Sprague Dawley rats were randomized into three groups: non-MI/R group (Sham, n = 15), MI/R group treated with vehicle (Control, n = 15) and MI/R group treated with GXST (Drug, n = 15). MI/R was induced by ligation of the left anterior descending coronary artery (LAD) for 30 minutes, followed by 2/24 hour reperfusion in the Control and Drug groups. In the Sham group, the LAD was exposed without occlusion. GXST powder (in the Drug group) or saline (in the Control and Sham groups) were administered via direct gastric gavage from 7 day prior to surgery. Blood samples were collected from the carotid artery (10 rats each group) after 2 hours of reperfusion, to determine the levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1) using enzyme-linked immunosorbent assays. The animals were then sacrificed and the hearts were harvested for histopathology and western blot analysis. Infarct size was measured in the remaining five rats in each group after 24 hours reperfusion. Results GXST significantly decreased levels of TNF-α, IL-1β, IL-6, ICAM-1, apoptosis index (AI) and infarct size. GXST also obviously inhibited nuclear factor kappa B (NF-κB) activity when compared with the Control group (all P < 0.05). Conclusions GXST is effective in protecting the myocardium against MI/R injury in rats. Its possible cardioprotective mechanism involves inhibition of the inflammatory response and apoptosis following MI/R injury.

Objective To study the effect of Pioglitazone(PIO) on intimal hyperplasia after vein graft and its potential mechanism.Methods 32 male Sprague-Dawley rats were randomly divieded into two groups,one admisnistrated with PIO(3 mg· kg-1 · d-1) and the other with saline.A week later,the right common carotid arteries were reconstructed using homolateral external jugular veins in rats.The drugs treatment was continued after surgery for 2 or 4 weeks until grafted veins were harvested.The neointima thickness was measured by Computer image analysis software.To observe the activation of ERK1/2 pathway,the western blot were performed.In vitro,human great saphenous vein smooth muscle cells were co-cultured with PIO,and cells proliferation was detected by the CCK-8 assay.The TUNEL staining was performed to determine apoptosis.Results PIO treatment significantly attenuated intimal thickening compared with the the control group both at second [(8.56 ± 1.64) μm vs (25.44 ± 0.89) μm,P ＜ 0.01] and fourth week [(10.51 ± 1.47) μm vs (35.69 ± 1.07) μm,P ＜ 0.01)] after veins graft.Also PIO inhibited the ERK1/2 activation in grafted veins.In vitro,PIO significantly reduced PDGF-induced cells proliferation and increased cells apoptosis.Conclusion PIO effectively improved intimal hyperplasia in grafted veins perhaps associated with its ability to suppress vascular smooth muscle cells proliferation and enhance cell apoptosis,and might be related to the down regulation of ERK1/2 activity.