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Therapeutic concentrations of propofol protects mouse macrophages from nitric oxide-induced cell death and apoptosis

[Des concentrations thérapeutiques de propofol protègent les macrophages de souris de la mort cellulaire et de l'apoptose induites par l'oxyde nitrique]

Hang Chang, MD PhD^*, Shih-Ying Tsai, MS, Yi Chang, MD^*, Ta-Liang Chen, MD PhD and Ruei-Ming Chen, PhD

^* From the Departments of Education and Research, Shin-Kong Wu Ho-Su Memorial Hospital; Surgery and Anesthesiology,
College of Medicine; Physiology and Graduate Institute of Medical Science,
College of Medicine; and Anesthesiology, Wan-Fang Hospital, College of Medicine Taipei Medical University, Taipei, Taiwan.

Address correspondence to: Dr. Ruei-Ming Chen, Department of Anesthesiology, Wan-Fang Hospital, College of Medicine, Taipei Medical University, No. 111, Sec. 3, Hsing-Lung Rd., Taipei, 116, Taiwan. Phone: 886-2-29307930, ext. 2159; Fax: 886-2-86621150; E-mail: rmchen{at}tmu.edu.tw

Purpose: To evaluate the potential effect of a clinically relevant concentration of propofol (PPF) on cell viability and nitric oxide-induced macrophage apoptosis.

Methods: Mouse macrophages (cell line Raw 264.7) were cultured and incubated with a nitric oxide donor sodium nitroprusside (SNP), PPF, and a combination of PPF and SNP for one, six and 24 hr. Cell viability was determined by the colorimetric 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptotic cells were determined by analyzing the percentages of sub-G1 phase in macrophages. The amounts of nitric oxide were assayed.

Results: The amounts of nitric oxide in macrophages were increased with time when incubated with SNP (P < 0.05). Simultaneously, SNP caused cell death of macrophages in a concentration-and time-dependent manner (P < 0.05). PPF per se did not alter the amount of basal and SNP-provided nitric oxide in macrophages. A therapeutic concentration of PPF (30 µM) exhibited no cytotoxicity. After incubation with SNP for one and six hours, PPF could completely or partially block nitric oxide-induced cell death, respectively (P < 0.05).

Administration of SNP to macrophages resulted in a time-dependent pattern of increase of apoptotic cells (P < 0.05). Similar to the results of the cell viability analyses, PPF was able to protect macrophages from nitric oxide-induced apoptosis in one and six hour-treated groups (P < 0.05) but not in the 24 hr treated group.

Conclusion: PPF, at a therapeutic concentration, can protect mouse macrophages in vitro from nitric oxide-induced cell apoptosis as well as cell death.

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