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Propofol attenuates Kupffer cell activation during hypoxia-reoxygenation

[Le propofol diminue l’activation des cellules de Kupffer pendant l’hypoxie-réoxygénation]

Eon-Gi Sung, MD, PhD^*, Daelim Jee, MD^*, In-Hwan Song, MD, PhD^*, Hee-Sun Kim, MD, PhD^*, Jae Hoon Bae, MD, PhD and Se-Hun Park, MD

^* From the Kupffer Cell Research Group Yeungnam University College of Medicine, Daegu;
the Department of Physiology, Keimyung University School of Medicine, Daegu; and
the Department of Anesthesiology, Ulsan University Hospital, College of Medicine, University of Ulsan, Ulsan, Korea.

Address correspondence to: Dr. Daelim Jee, Department of Anesthesiology, Yeungnam University College of Medicine, Daemyung-Dong, Nam-Gu, Daegu, Korea 705-035. Phone: 82-53-620-3367; Fax: 82-53-626-5275; E-mail: djee{at}med.yu.ac.kr

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)- mRNA, and KC viability were measured in response to hypoxia-reoxygenation following pretreatment with propofol 0.5 and 5 µg·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- 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- 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.