Details

Autor(en) / Beteiligte

• Guo, Yi
• Wang, Qi-zhang
• Li, Fang-ming
• Jiang, Xin
• Zuo, Yan-fang
• Wang, Ling

Titel

Biochemical pathways in the antiatherosclerotic effect of berberine

Ist Teil von

• Chinese medical journal, 2008-07, Vol.121 (13), p.1197-1203

Ort / Verlag

China: Department of Neurology, Second Affiliated Hospital of Jinan University, Shenzhen, Guangdong 518020,China%Department of Neurology, Affiliated Shenzhen Shajing Hospital of Guangzhou Medical College, Shenzhen, Guangdong 518104 China%Department of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430030,China%Department of Cardiology, Second Affiliated Hospital of Jinan University, Shenzhen, Guangdong 518020,China

Erscheinungsjahr

2008

Quelle

MEDLINE

Beschreibungen/Notizen

• 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 up to 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 （P 〈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, SP600125 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.