Publications (5)13.11 Total impact

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    ABSTRACT: The 5-lipoxygenase catalyzed formation of leukotriene lipid mediators is a mediator for inflammatory response in arteries. The present study investigated the relationship between atorvastatin and the 5-lipoxygenase pathway in an atherosclerotic rabbit model. Thirty male New Zealand White Rabbits were randomized into negative control, positive control and atorvastatin groups. At week 4, the rabbits were subjected to carotid balloon-dilation injury or carotid balloon-dilation injury, followed by treatment with atorvastatin. At week 12, all the animals were sacrificed. Plasma lipids, LTD(4), and 15-epi-lipoxin A(4) were measured using the enzymatic endpoint method and ELISA, respectively. RT-PCR was performed to detect the gene expression of 5-lipoxygenase-activating protein and cysLT1R in rabbit carotid arteries. Finally, histological analysis was used to evaluate the pathophysiological changes of rabbit carotid arteries. The results showed atorvastatin markedly lowered serum lipids and LTD(4) levels compared with the control group. Similarly, mRNA expression of 5-lipoxygenase-activating protein and cysLT1R was significantly inhibited by atorvastatin. Decreased carotid plaque instability was evident in atorvastatin-treated animals, as demonstrated by a thickened elastic layer, less neointima hyperplasia and macrophage proliferation. Atorvastatin may stabilize carotid plaque by regulating the 5-lipoxygenase pathway in atherosclerotic rabbits and delay the progression of atherosclerosis by exerting anti-inflammatory effects.
    Cardiology 03/2010; 115(3):221-8. DOI:10.1159/000296017 · 2.18 Impact Factor
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    ABSTRACT: Matrix metalloproteinases (MMPs) play important roles in the development and destabilization of atherosclerotic plaques. It is known that montelukast inhibits neointimal hyperplasia. However, the underlying mechanisms for the inhibitory effects of montelukast on neointimal formation have been poorly defined. Thirty-six male New Zealand White rabbits were randomized as normal control, placebo (0.9% NaCl, 1.5 ml/kg/day, via intraperitoneal injection), atorvastatin (atorvastatin, 1.5 mg/kg/day, orally) and montelukast groups (montelukast, 1.5 mg/kg/day, via intraperitoneal injection). Atherosclerosis was induced by balloon-injury and high-cholesterol (HC) diet. Serum lipids were measured at 0, 8 and 12 weeks. After 12 weeks, the rabbits were sacrificed and histopathological changes examined. Immunohistochemistry and reverse transcription-polymerase chain reaction were used to measure the expression of MMP-2 and MMP-9 in the plaques. It was found that montelukast reduced neointimal formation, decreased macrophage accumulation, and increased smooth muscle cells. It also attenuated the expression of MMP-2 and MMP-9 in atherosclerotic plaques, but it had no effect on plasma lipid levels. These data indicate that montelukast inhibits neointimal hyperplasia in association with decreased expression of MMP-2 and MMP-9 independent of plasma lipid levels in atherosclerotic plaques after vascular injury in hyperlipidemic rabbits.
    Cardiovascular Drugs and Therapy 12/2009; 23(6):431-7. DOI:10.1007/s10557-009-6211-6 · 3.19 Impact Factor
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    ABSTRACT: Atherosclerosis is characterized by inflammatory responses of the arterial wall to "injury", which is prominently driven by inflammatory mediators. Montelukast, a selective CysLT1 receptor antagonist, has potent anti-inflammatory effects in diverse animal models. However, the role of montelukast in regulating inflammatory progression of atherosclerosis has not been elucidated. Therefore, we investigated the effect of montelukast on atherosclerosis compared with that of atorvastatin. Twenty-six male New Zealand White rabbits were randomized into four groups including a negative control group. The rabbits were fed a normal diet or an atherogenic diet for 12 weeks. The rabbits, except the negative control group, received right carotid artery balloon-injury 2 weeks after initiation of the atherogenic diet. Animals were then treated with montelukast (1mg/kg/day), atorvastatin (1.5mg/kg/day) or placebo for 4 weeks, respectively. At the end of the treatment, animals were killed and carotids were dislodged and detected. The results indicated that the placebo group had significant progression of atherosclerosis compared with the negative control group. In contrast, montelukast or atorvastatin treated rabbits showed a significant reduction of neointima, decreased macrophage content, increased SMC content and inhibited expression of MCP-1. Between two drugs, there were no significant differences in reducing neointima and decreasing the level of MCP-1. However, montelukast had no influence on plasma lipids, while atorvastatin down-regulated the levels of TC, TG and LDL. These results suggest that montelukast produces anti-atherogenic effects unrelated to plasma lipid modulation but related to MCP-1 down regulation.
    Atherosclerosis 12/2008; 205(1):74-9. DOI:10.1016/j.atherosclerosis.2008.11.012 · 3.99 Impact Factor
  • H.-B. Chen · D.-Z. Liu · S. Ge · G.-L. Xu · X.-F. Liu ·
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    ABSTRACT: Objective: To investigate the pathogenesis of middle cerebral artery(MCA) stenosis and occlusion caused cerebral infarction by a contrast study on atherosclerotic stenosis and occlusion of the main stem of MCA caused cerebral infarction in different MCA blood supplied areas and to provide evidence for the relative therapeutic strategies. Methods: The clinical and imaging data of 61 patients with fresh cerebral infarction caused by atherosclerotic MCA stenosis(stenosis >50%) and occlusion were analyzed retrospectively. The patients were divided into stenosis group(n = 27) and occlusion group(n = 34). The locations of cerebral infarction were determined and compared according to the results of MRI diffusion-weighted imaging(DWI) within one week after onset. Results: Single infarction in the stenosis and occlusion groups were 15(55.6%) and 8(23.5%) patients, respectively, and the multiple infarctions in the two groups were 12(44.4%) and 26(76.5%) patients, respectively (P < 0.05). Among the patients with single infarctions, the small perforating infarct(SPAI) in the stenosis and occlusion groups were 11 (11/15) and 2(2/8) patients(P = 0.039); among the patients with multiple infarctions, the perforating artery infarct(PAI) complicated with cortical infarction(pial infarct, PI) were 7(7/12) and 3(3/26) patients(P = 0.005); among the patients with multiple infarctions, PAI complicated with PI and border-zone infarct(BZI) were 1(1/12) and 16(16/ 26) patients(P = 0.004); there were 5 and 23 patients with BZI(P < 0.001). Conclusions: The sites of cerebral infarction caused by atherosclerotic stenosis and occlusion of main-stem of MCA has significant difference. It is suggested that there are different pathogenesis between them. Cerebral infarction caused by MCA stenosis may be resulted from the ostial lesion of the perforating artery and embolism. The former caused more single infarctions and the latter caused more multiple infarctions.
    Chinese Journal of Cerebrovascular Diseases 06/2008; 5(6):241-245.
  • H. Chen · S. Ge · G. Xu · X. Liu · R. Zhang · Q. Yin ·

    Cerebrovascular Diseases 01/2007; 24(6):490-490. · 3.75 Impact Factor