PMID- 20606305
OWN - NLM
STAT- MEDLINE
DCOM- 20101126
LR  - 20190720
IS  - 1347-5215 (Electronic)
IS  - 0918-6158 (Linking)
VI  - 33
IP  - 7
DP  - 2010
TI  - Cytokine reducing effect of azelnidipine in human peripheral blood mononuclear 
      cells.
PG  - 1148-51
AB  - Numerous clinical trials have shown that calcium channel blocker (CCB) therapy 
      improves the clinical outcome in patients with cardiovascular diseases. Since the 
      progression of several types of cardiovascular diseases is closely associated 
      with inflammation, alleviation of inflammation may be one potential mechanism of 
      those beneficial effects of CCB therapy. We examined whether a new CCB 
      (azelnidipine) could influence the inflammatory response of human peripheral 
      blood mononuclear cells (PBMCs), which are recruited to inflammatory lesions and 
      modulate inflammation. We investigated whether azelnidipine affected 
      intracellular signaling and cytokine production by phytohemagglutinin 
      (PHA)-stimulated human PBMCs in vitro. PBMCs were obtained from 10 healthy 
      volunteers and stimulated with PHA. Then relative intracellular calcium ion 
      concentration ([Ca(2+)](i)) was assessed by fluorescence microscopy, and the 
      production of monocyte chemoattractant protein-1 (MCP-1) and tumor necrosis 
      factor-alpha (TNF-alpha) were measured by enzyme-linked immunosorbent assay. 
      Stimulation with PHA significantly raised [Ca(2+)](i) and enhanced the production 
      of MCP-1 and TNF-alpha by human PBMCs. Azelnidipine significantly diminished the 
      PHA-induced rise of [Ca(2+)](i), and the production of MCP-1 and TNF-alpha. These 
      findings indicate that azelnidipine might have an anti-inflammatory influence on 
      human PBMCs, although the mechanisms and the difference from other CCBs still 
      remain unclear and further exploration should be required.
FAU - Miura, Ryuzea
AU  - Miura R
AD  - Department of Cardiovascular Medicine, Graduate School of Medicine, Dentistry and 
      Pharmaceutical Sciences, Okayama University, Okayama, Japan. 
      ryuzeamiura@mail.goo.ne.jp
FAU - Nakamura, Kazufumi
AU  - Nakamura K
FAU - Miura, Daiji
AU  - Miura D
FAU - Miura, Aya
AU  - Miura A
FAU - Kajiya, Masahito
AU  - Kajiya M
FAU - Hisamatsu, Kenichi
AU  - Hisamatsu K
FAU - Nagase, Satoshi
AU  - Nagase S
FAU - Morita, Hiroshi
AU  - Morita H
FAU - Kusano, Kengo Fukushima
AU  - Kusano KF
FAU - Matsubara, Hiromi
AU  - Matsubara H
FAU - Ohe, Tohru
AU  - Ohe T
FAU - Ito, Hiroshi
AU  - Ito H
LA  - eng
PT  - Journal Article
PL  - Japan
TA  - Biol Pharm Bull
JT  - Biological & pharmaceutical bulletin
JID - 9311984
RN  - 0 (Calcium Channel Blockers)
RN  - 0 (Cytokines)
RN  - 0 (Dihydropyridines)
RN  - 0 (Inflammation Mediators)
RN  - 5GZ3E0L9ZU (Azetidinecarboxylic Acid)
RN  - PV23P19YUG (azelnidipine)
SB  - IM
MH  - Azetidinecarboxylic Acid/*analogs & derivatives/pharmacology
MH  - Calcium Channel Blockers/*pharmacology
MH  - Cytokines/*blood
MH  - Dihydropyridines/*pharmacology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Humans
MH  - Inflammation Mediators/*blood
MH  - Monocytes/*drug effects/metabolism
EDAT- 2010/07/08 06:00
MHDA- 2010/12/14 06:00
CRDT- 2010/07/08 06:00
PHST- 2010/07/08 06:00 [entrez]
PHST- 2010/07/08 06:00 [pubmed]
PHST- 2010/12/14 06:00 [medline]
AID - JST.JSTAGE/bpb/33.1148 [pii]
AID - 10.1248/bpb.33.1148 [doi]
PST - ppublish
SO  - Biol Pharm Bull. 2010;33(7):1148-51. doi: 10.1248/bpb.33.1148.