当归芍药散对代谢性炎性反应小鼠血脂和血清炎性反应因子IL-6、MCP-1及NF-κB、PPARγmRNA表达的影响

doi:10.3969/j.issn.1006-7795.2014.06.025

首都医科大学学报 ›› 2014, Vol. 35 ›› Issue (6): 813-817.doi: 10.3969/j.issn.1006-7795.2014.06.025

当归芍药散对代谢性炎性反应小鼠血脂和血清炎性反应因子IL-6、MCP-1及NF-κB、PPARγmRNA表达的影响

贾丽超, 周明学, 张蕾, 刘卫红

首都医科大学附属北京中医医院北京市中医研究所, 北京 100010

收稿日期:2014-04-21 发布日期:2014-12-15
通讯作者: 刘卫红 E-mail:wh.l-007@163.com
基金资助:
北京市自然科学基金(7142037),北京市卫生系统高层次卫生技术人才培养计划资助

Effect of Dangguishaoyaosan on the blood lipids and the expression of inflammatory factors, such as IL-6, MCP-1, NF-κB and PPAR-γmRNA in the metaflammatory mice

Jia Lichao, Zhou Mingxue, Zhang Lei, Liu Weihong

Institute of Traditional Chinese Medicine, Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing 100010, China

Received:2014-04-21 Published:2014-12-15
Supported by:
This study was supported by Natural Science Foundation of Beijing(7142037), High Level of Health Technical Personnel Training Plan of Beijing Municipal Health Financing System.

摘要/Abstract

摘要：

目的研究当归芍药散对代谢性炎性反应小鼠血脂和血清炎性反应因子白细胞介素-6(interleukin-6,IL-6)、单核细胞趋化蛋白-1(monocyte chemotactic protein 1,MCP-1)以及核因子κB (nuclear factor kappa B,NF-κB)和活化的过氧化物酶体增生物激活受体γ(peroxisome proliferator-activated receptor gamma,PPARγ)mRNA表达的影响。方法 60只雄性C57小鼠,采用数字表法将动物随机分为正常组、模型组、立普妥组、当归芍药散组(n=15)。采用高脂饮食联合脂多糖注射造成小鼠代谢性炎性反应模型。造模5周后,开始灌胃给药,每天2次,当归芍药散2.2 g/kg,立普妥0.003 g/kg。正常对照组和模型组灌服等体积蒸馏水。连续灌胃5周。处死后采血和取肝脏,检测各组小鼠血清胆固醇(total cholesterol,TC) 、三酰甘油(triglyceride,TG) 和低密度脂蛋白胆固醇(low density lipoprotein,LDL-C)浓度,并采用流式细胞术检测血清炎性反应因子IL-6和MCP-1浓度。反转录聚合酶链式反应(reverse transcription polymerase chain reaction,RT-PCR) 法测定肝脏NF-κB和PPARγmRNA的表达。结果与模型组相比,当归芍药散组小鼠血清TC和LDL-C水平明显降低(P<0.01),肝脏组织中NF-κB mRNA的表达降低,差异有统计学意义(P<0.05),PPARγmRNA的表达提高,差异有统计学意义(P<0.05)。结论当归芍药散可降低代谢性炎性反应小鼠血脂和血清炎性反应因子IL-6和MCP-1浓度,并可通过调控核转录因子NF-κB和PPARγ受体,抑制小鼠体内代谢性炎性反应,从而可能对早期动脉粥样硬化起到干预作用。

关键词: 当归芍药散, 代谢性炎性反应, 脂代谢紊乱, 动脉粥样硬化

Abstract:

Objective To study the effect of Dangguishaoyaosan on the blood lipids and the expression of inflammatory factors, such as IL-6, MCP-1, NF-κB and PPAR-γ mRNA in the metaflammatory mice. Methods Sixty male C57 mice were randomly divided into normal group, model group, the lipitor group and Dangguishaoyaosan group(n=15). High-fat diets joining lipopolysaccharide injection were used to build the metabolic inflammatory model in mice. Five weeks later, all groups in addition to the normal were given a gavage twice a day for five weeks,according to the dose conversed from the clinical equivalent dose. When the test was finished, we collect the blood and liver, test the serum cholesterol(TC), triglyceride(TG) and low density lipoprotein cholesterol(LDL-C) level, using flow cytometry to detect the serum level of IL-6 and MCP-1. Reverse transcription polymerase chain reaction(RT-PCR) was used to detect the expression of NF-κB and PPAR-γ mRNA in liver. Results Compared with the model group,the serum TC and LDL-C level of Dangguishaoyaosan group significantly decreased(P<0.01), and the expression of NF-κB mRNA in liver tissue decreased significantly(P<0.01), while the expression of PPAR-γmRNA significantly increased(P<0.01). Conclusion Dangguishaoyaosan can reduce the blood lipid, IL-6 and MCP-1 level of metabolic inflammation mice, and can influence metabolic inflammation in mice, which might have an intervention effect on the early atherosclerosis through regulating nuclear transcription factor NF-κB and PPAR-γ receptors.

Key words: Dangguishaoyaosan, metaflammation, dyslipidemia, atherosclerosis

中图分类号:

R285.5

贾丽超, 周明学, 张蕾, 刘卫红. 当归芍药散对代谢性炎性反应小鼠血脂和血清炎性反应因子IL-6、MCP-1及NF-κB、PPARγmRNA表达的影响[J]. 首都医科大学学报, 2014, 35(6): 813-817.

Jia Lichao, Zhou Mingxue, Zhang Lei, Liu Weihong. Effect of Dangguishaoyaosan on the blood lipids and the expression of inflammatory factors, such as IL-6, MCP-1, NF-κB and PPAR-γmRNA in the metaflammatory mice[J]. Journal of Capital Medical University, 2014, 35(6): 813-817.

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当归芍药散对代谢性炎性反应小鼠血脂和血清炎性反应因子IL-6、MCP-1及NF-κB、PPARγmRNA表达的影响

Effect of Dangguishaoyaosan on the blood lipids and the expression of inflammatory factors, such as IL-6, MCP-1, NF-κB and PPAR-γmRNA in the metaflammatory mice

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