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Biochemical pathways in the antiatherosclerotic effect of berberine

GUO Yi WANG Qi-zhang LI Fang-ming JIANG Xin ZUO Yan-fang WANG Ling

中华医学杂志(英文版)2008,Vol.121Issue(13):1197-1203,7.
中华医学杂志(英文版)2008,Vol.121Issue(13):1197-1203,7.

Biochemical pathways in the antiatherosclerotic effect of berberine

Biochemical pathways in the antiatherosclerotic effect of berberine

GUO Yi 1WANG Qi-zhang 2LI Fang-ming 3JIANG Xin 4ZUO Yan-fang 1WANG Ling1

作者信息

  • 1. Department of Neurology, Second Affiliated Hospital of Jinan University, Shenzhen, Guangdong 518020,China
  • 2. Department of Neurology, Affiliated Shenzhen Shajing Hospital of Guangzhou Medical College, Shenzhen, Guangdong 518104 China
  • 3. Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030,China
  • 4. Department of Cardiology, Second Affiliated Hospital of Jinan University, Shenzhen, Guangdong 518020,China
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摘要

Abstract

Background This study investigated the inhibitory effect of berberine(BBR)on lipopolysaccharide(LPS)induced cyclooxygenase-2(COX-2)expression via the mitogen activated protein kinase(MAPK)signalling cascade pathways in human peripheral blood monocytes(PBMC).Methods PBMC from whole blood were isolated and cultured for uD 10 24 hours after division into 5 groups treated with LPS,LPS+BBR 25 μmol/L,LPS+BBR 50 μmol/L or LPS+BBR 100 μmol/L and untreated.Monocytes were extracted for RT-PCR and Western blot analyses to examine COX-2 mRNA and protein activated expression of p38 mitogen activated protein kinase(p38MAPK),Jun N-terminal kinase(JNK)and extracellular regulated kinases 1/2(ERK1/2)signalling pathways.Results COX-2 mRNA and protein expression decreased to a minimum at 12 hours after BBR treatment fP<0.05).With the increasing concentration of BBR treatment,the COX-2 expression decreased progressively(P<0.01).With BBR treatment for 6,12 or 24 hours at three doses,ERK1/2 protein expression was significantly inhibited.For the JNK pathway,only with the treatment of BBR at the concentration of 100 μmol/L was JNK protein expression inhibited compared with the LPS stimulation group(P<0.01).Irrespective of the BBR concentration,no difference was shown between the BBR group and the LPS group for p38MAPK protein expression.Human monocytes COX-2 mRNA,by RT-PCR,and protein expression,by Western blot analysis,were inhibited when incubated with PD98059,SP6001 25 and SB203580 (P<0.05).Conclusions Berberine inhibits COX-2 expression via the ERK1/2 signalling pathway and,possibly,at a high dosage via the JNK pathway.P38MAPK may have no relationship with the effect of BBR in PBMC.Berberine inhibited COX-2 mRNA and protein expression in a dose dependent manner and suppressed COX-2 expression to a minimal level after 12 hours of berberine treatment.

关键词

antiatherosclerotic/berberine/cyclooxygenase/erk1/2/jnk/p38mapk

Key words

antiatherosclerotic/berberine/cyclooxygenase/erk1/2/jnk/p38mapk

分类

医药卫生

引用本文复制引用

GUO Yi,WANG Qi-zhang,LI Fang-ming,JIANG Xin,ZUO Yan-fang,WANG Ling..Biochemical pathways in the antiatherosclerotic effect of berberine[J].中华医学杂志(英文版),2008,121(13):1197-1203,7.

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