参七脉心通胶囊对颈动脉粥样硬化患者单核细胞相关因子的影响
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摘要
目的:通过观察治疗前后颈动脉粥样硬化患者血清单核细胞趋化蛋白1(MCP-1)及巨噬细胞集落刺激因子(M-CSF)的变化,探讨参七脉心通胶囊抗动脉粥样硬化的可能机制。方法:符合纳入标准的90例颈动脉粥样硬化患者随机分为观察组及对照组各45例。对照组给予辛伐他汀治疗,观察组给予参七脉心通胶囊及辛伐他汀治疗,疗程共24周,治疗前检测血清MCP-1、M-CSF、低密度脂蛋白胆固醇(LDL-C)、总胆固醇(TC)及内中膜厚度(IMT)等指标,12周后复查LDL-C、TC及IMT,24周后复查血清MCP-1、M-CSF、LDL-C、TC及IMT,评估比较两组差异。结果:治疗12周后,两组患者LDL-C及TC明显下降,与治疗前比较,差异具有统计学意义(P<0.05);治疗24周后,两组患者MCP-1、M-CSF及IMT明显下降,与治疗前比较,差异具有统计学意义(P<0.05);而且,观察组MCP-1、M-CSF、LDL-C、TC及IMT较对照组明显下降,差异具有统计学意义(P<0.05)。结论:参七脉心通胶囊不仅能够调节血脂代谢,而且发现其抗动脉粥样硬化作用的机制可能与减轻单核细胞募集程度相关,在临床应用安全有效。
Objective:To explore the mechanism of Shenqi Maixintong Capsule for anti-carotid atherosclerosis by observing the effect of Shenqi Maixintong Capsule on the serum monocyte chemoattractant protein-1(MCP-1) and macrophage colony-stimulating factor(M-CSF) in patients with carotid atherosclerosis. Methods:Ninety patients with carotid atherosclerosis were divided into observation group and control group randomly,with 45 cases in each group. Patients in the observation group were treated with Shenqi Maixintong Capsule and simvastatin,while patients in the control group were treated with simvastatin. Both groups were treated for 24 weeks. Before the treatment,serum MCP-1,M-CSF,low density lipoprotein cholesterol(LDL-C),total cholesterol(TC) and carotid intima-media thickness(IMT) were tested,after 12 weeks of treatment,serum LDL-C,TC and IMT were tested again,and after 24 weeks of treatment,serum MCP-1,M-CSF,LDL-C,TC and IMT were tested again. The difference between two groups was compared. Results:After 12 weeks of treatment,LDL-C and TC of the two groups decreased significantly and showed statistical difference compared with before treatment(P<0.05). After 24 weeks of treatment,MCP-1,M-CSF and IMT of the two groups decreased significantly and showed statistical difference compared with before treatment(P<0.05). MCP-1,M-CSF,LDL-C,TC and IMT of the observation group decreased more obviously than those of the control group,with statistical difference(P<0.05). Conclusions:Shenqi Maixintong Capsule can regulate blood lipid metabolism,and the mechanism of anti-atherosclerosis may be related to reducing the degree of monocyte recruitment. This capsule is safe and effective in clinical application.
Objective:To explore the mechanism of Shenqi Maixintong Capsule for anti-carotid atherosclerosis by observing the effect of Shenqi Maixintong Capsule on the serum monocyte chemoattractant protein-1(MCP-1) and macrophage colony-stimulating factor(M-CSF) in patients with carotid atherosclerosis. Methods:Ninety patients with carotid atherosclerosis were divided into observation group and control group randomly,with 45 cases in each group. Patients in the observation group were treated with Shenqi Maixintong Capsule and simvastatin,while patients in the control group were treated with simvastatin. Both groups were treated for 24 weeks. Before the treatment,serum MCP-1,M-CSF,low density lipoprotein cholesterol(LDL-C),total cholesterol(TC) and carotid intima-media thickness(IMT) were tested,after 12 weeks of treatment,serum LDL-C,TC and IMT were tested again,and after 24 weeks of treatment,serum MCP-1,M-CSF,LDL-C,TC and IMT were tested again. The difference between two groups was compared. Results:After 12 weeks of treatment,LDL-C and TC of the two groups decreased significantly and showed statistical difference compared with before treatment(P<0.05). After 24 weeks of treatment,MCP-1,M-CSF and IMT of the two groups decreased significantly and showed statistical difference compared with before treatment(P<0.05). MCP-1,M-CSF,LDL-C,TC and IMT of the observation group decreased more obviously than those of the control group,with statistical difference(P<0.05). Conclusions:Shenqi Maixintong Capsule can regulate blood lipid metabolism,and the mechanism of anti-atherosclerosis may be related to reducing the degree of monocyte recruitment. This capsule is safe and effective in clinical application.
引文
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[12]范如宇,丁碧云.动脉粥样硬化易损斑块的中医药研究进展[J].安徽医药,2012,16(4):537-539.
[2]MONTERO VEGA M T.The inflammatory process underlying atherosclerosis[J].Crit Rev Immunol,2012,32(5):373-462.
[3]陈朝俊,付强,黄卫江.参七脉心通胶囊对树突状细胞抗原递呈相关内皮损伤因子的影响[J].广东医学,2009,30(6):888-889.
[4]WEBER C,NOELS H.Atherosclerosis:current pathogenesis and therapeutic options[J].Nature Medicine,2011(17):1410-1422.
[5]GALKINA E,LEY K.Immune and inflammatory mechanisms of atherosclerosis[J].Annual Review of Immunology,2009(27):165-197.
[6]DESHMANE SL,KREMLEY S,AMINI S,et al.Monocyte chemoattractant protein-1(MCP-1):an overview[J].Journal of Interferon and Cytokine Research,2009,29(6):313-326.
[7]DAWSON J,MILTZ W,MIR A K,WIESSNER C.Targeting monocyte chemoattractant protein-1 signalling in disease[J].Expert Opinion on Therapeutic Targets,2003(7):35-48.
[8]BORING L,GOSLING J,CLEARY M,CHARO I F.Decreased lesion formation in CCR2-/-mice reveals a role for chemokines in the initiation of atherosclerosis[J].Nature,1998(394):894-897.
[9]CONWAY JG,MCDONALD B,PARHAM J,et al.Inhibition of colony-stimulating-factor-1 signaling in vivo with the orally bioavailable cFMS kinase inhibitor GW2580[J].Proceedings of the National Academy of Science of the United States of America,2005(102):16078-16083.
[10]VIVEK Mishra,SATYESH K Sinha,TRIPATHI B Rajavashisth.Role of macrophage colony-stimulating factor in the development of neointimal thickening following arterial injury[J].Cardiovascular Pathology,2016(25):284-292.
[11]诸骏仁,高润霖,赵水平,等.中国成人血脂异常防治指南(2016年修订版)[J].中国循环杂志,2016,44(10):833-853.
[12]范如宇,丁碧云.动脉粥样硬化易损斑块的中医药研究进展[J].安徽医药,2012,16(4):537-539.