Article Summary
张云霞赵钢△ 史明周林甫.人参皂甙Rd 抑制大鼠局灶性脑缺血后趋化因子CXCL1 和 γ- 干扰素的蛋白表达[J].现代生物医学进展英文版,2011,11(6):1059-1062.
人参皂甙Rd 抑制大鼠局灶性脑缺血后趋化因子CXCL1 和 γ- 干扰素的蛋白表达
Ginsenoside-Rd Inhibits CXCL1 and Interferon-γProtein Expressionsin Rats after Focal Cerebral Ischemia
  
DOI:
中文关键词: 人参皂甙Rd  液相芯片  趋化因子CXCL1  γ- 干扰素
英文关键词: Ginsenoside-Rd  Luminex xMAP technology  CXCL1  IFN-γ
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Author NameAffiliation
ZHANG Yun-xia, ZHAO Gang△, SHI Ming, ZHOU Lin-fu 第四军医大学附属西京医院神经内科 
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中文摘要:
      目的:研究人参皂甙Rd(Ginsenoside-Rd,GS-Rd)在大鼠局灶性脑缺血后对炎症趋化因子CXCL1 和γ- 干扰素(Interferon-γ, IFN-γ)的影响。方法:将SD 大鼠随机分为5 组:正常组(n=5),假手术组(n=5),GS-Rd 对照组(n=5),大脑中动脉栓塞模型 (MCAO)组(n=20),MCAO+GS-Rd 组(n=20)。正常组不做任何处理;假手术组进行大脑中动脉栓塞手术,但不插入栓线;GS-Rd 对照组给予腹腔注射10 mg/Kg GS-Rd,不进行手术;MCAO 组(n=20)和MCAO+ GS-Rd 组(n=20)进行大脑中动脉栓塞手术,术 后2 小时拔出栓线,MCAO+ GS-Rd 组在术前15 分钟腹腔注射10 mg/Kg GS-Rd。在12 小时、1 天、3 天、7 天四个时间点分别提取 脑组织蛋白,通过液相芯片技术检测CXCL1,IFN-γ 含量。结果:正常组,假手术组和GS-Rd 对照组组间CXCL1,IFN-γ 含量无 统计学差异;与三个对照组相比,MCAO 组和MCAO+ GS-Rd 组中CXCL1,IFN-γ蛋白含量均有明显增加(P<0.05);而与MCAO 组相比,MCAO+ GS-Rd 组CXCL1,IFN-γ的生成明显减少(P<0.05)。结论:10 mg/Kg GS-Rd 预处理可有效抑制大鼠短暂性脑缺 血后CXCL1,IFN-γ的生成;通过抑制炎症反应,GS-Rd 可能在神经保护中发挥重要的作用。
英文摘要:
      Objective: To investigate the effect of Ginsenoside-Rd (GS-Rd) on protein expression of CXCL1 and IFN-γ(interferon- γ, IFN-γ)in rats after focal cerebral ischemia. Methods: A total of 55 rats were randomly divided into the five groups: blank group (n=5); Sham group (n=5),with surgery but no occlusion; GS-Rd group (n=5),with 10 mg/kg GS-Rd treatment but no surgery; middle cerebral artery occlusion(MCAO) group (n=20),with vehicle application before surgery; MCAO+GS-Rd group (n=20),with 10 mg/kg GS-Rd treatment before MCAO. After 2 h of occlusion, the suture was carefully removed to restore blood flow. Then the brain protein were extracted respectively at 12hour, 1day, 3day, 7day and were tested by LUMINEX 200. Results: Our results showed that the protein levels of CXCL1 and IFN-γwere significantly increased afterMCAO insult at all time points (p<0.05). Pretreatment of 10 ml/kg GS-Rd inhibited MCAO-induced protein expressions of CXCL1 and IFN-γ(p<0.05). Conclusion: These results suggest that neuroprotection of GS-Rd following cerebral ischemia may be at least due to inhibition of the proteins expression of CXCL1 and IFN-γ.
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