Propofol attenuates Kupffer cell activation during hypoxia-reoxygenation [Le propofol diminue ľactivation des cellules de Kupffer pendant ľhypoxie-réoxygénation]

Authors
Eon-Gi SungDaelim JeeIn-Hwan SongHee-Sun KimJae Hoon BaeSe-Hun Park
Department
Dept. of Physiology (생리학)
Issue Date
2005
Citation
Canadian Journal of Anesthesia, Vol.52(9) : 921-926, 2005
ISSN
0832-610X
Abstract
PURPOSE: We undertook a study to determine whether propofol may attenuate Kupffer cell (KC) activation, thus protecting the cells against hypoxia-reoxygenation injury through the modulation of intracellular calcium ([Ca2+]i). METHODS: [Ca2+]i, the expression of tumour necrosis factor (TNF)-alpha mRNA, and KC viability were measured in response to hypoxia-reoxygenation following pretreatment with propofol 0.5 and 5 microg.mL(-1) (Groups P1 and P2, respectively) or without propofol (Group HRC). KCs were isolated and cultured from male Sprague-Dawley rats. KCs were incubated under an atmosphere of hypoxia (95% N2 + 5% CO2) for 60 min with subsequent 120 min reoxygenation (95% air + 5% CO2). [Ca2+]i for the first 12 min after reoxygenation, TNF-alpha mRNA, and KC viability at the end of reoxygenation in groups P1 and P2 were compared with those of HRC. RESULTS: The increase of [Ca2+]i from the baseline was attenuated in P1 (96.6 +/- 6.9%) and P2 (96.1 +/- 5.4%) compared with HRC (143.8 +/- 11.5%), (P < 0.001), with no difference between P1 and P2. The expression of TNF-alpha mRNA increased only in HRC during hypoxia-reoxygenation. KC viability increased in P1 (97.5 +/- 2.6%) and P2 (94.6 +/- 2.9%), compared with HRC (89.9 +/- 1.4%), (P < 0.005), with no difference between P1 and P2. CONCLUSION: The results indicate that propofol attenuates KC activation and protects KC from hypoxia-reoxygenation injury at clinically relevant concentrations. This attenuation seems to result from inhibition of [Ca2+]i increase in KC.
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/35276
Appears in Collections:
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Physiology (생리학)
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Full Text
http://lps3.link.springer.com.proxy.dsmc.or.kr/article/10.1007%2FBF03022052
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