JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2010, Vol. 48 ›› Issue (12): 120-.

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Effect of APS on TLR4、NF-κB expression in HUVEC-C injured by   patients blood with hypertension disease

ZHANG Jing-zhi1,  CHENG Li-guo2, HU Xiao-qin3, JIA Hui-xin4   

  1. 1. Department of Traditional Chinese Medicine, The Second Affiliated Hospital of GuangZhou Medicine College, 
    Guangzhou 510260, China; 2. School of Medicine,  Jinan University, Guangzhou 510632, China;
    3. GuangXi Traditional Chinese Medical College, Nanning 530001, China;  4. Department of Traditional Chinese Medicine,
    General Hospital of Daqing Oil Field Company, Daqing 163001, Heilongjiang, China
  • Received:2010-05-27 Published:2010-12-16

Abstract:

Objective     To investigate the effects of APS on TLR4、 NF-κB expression and signal pathway in vascular endothelial cells injured by hypertension patients′ blood. Methods     The human umbilical vein endothelial cells  (HUVEC-Cs) were intervened by 10% serum of  hypertension patient or healthy human for 24h.  TLR4mRNA expression in HUVEC-Cs was detected by real time PCR. After the lipopolysaccharide(LPS) activated HUVEC-Cs were effected by different dosage APS, TLR4 and NFκB mRNA were detected by real time PCR, TLR4 and NF-κB protein were detected by western blot. Results    After the serum acted the HUVEC-Cs for 24h, TLR4mRNA expression was increased in hypertension disease group than the healthy group(P<0.01). APS showed the ability of reducing TLR4mRNA expression, inhibiting TLR4 protein expression and suppressing  IκB protein degeneration in LPS activated HUVEC-Cs in a dose-dependent manner(P<0.05, P<0.01, P<0.001).  Conclusion    Inflammatory reaction and immunity disorder initiated by TLR-NF-κB signal pathway is one of the influencing mechanisms in the damage of vascular endothelial cells of hypertension disease. APS can reduce the damage.

Key words: Essential hypertension; Vascular endothelial cells; Toll-like receptor 4; Nuclear factorκB; Astragaluspolysaccharide

CLC Number: 

  • R544.1
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