摘要：

SUMMARYKetamine is commonly used in equine anaesthesia. Next to its anaesthetic and analgesic effects, ketamine has also been found to exhibit potent cytokine- modulating and antioxidative properties in rodents and humans. In addition, in an equine macrophage cell line (e-CAS cells), ketamine reduced lipopolysaccharide (LPS)-induced tumour necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) production in a concentration-dependent manner.1 In the present study, the antioxidative effects of ketamine in e-CAS cells were studied. Initially, two different ROS-inducers, LPS (1 μg/mL), phorbol myristate acetate (PMA; 1 μM) and the combination LPS (1 μg/mL)/PMA (1 μM) were tested. The capacity of ketamine (0-36 μM) to suppress reactive oxygen species (ROS) production in e-CAS cells was investigated by using 2',7'-dichlorodihydrofluorescein diacetate (H2DCF- DA) as a molecular probe. Furthermore, to determine the mechanism underlying the effect of ketamine on stimulated ROS production, the influence of ketamine on intracellular glutathione (GSH) concentrations was measured.In e-CAS cells, a significant increase in ROS formation was documented only following exposure to the combination LPS/PMA. Ketamine significantly and dose-dependently reduced ROS formation in LPS/PMA-stimulated e-CAS cells. In addition, ketamine significantly increased total intracellular GSH concentrations in LPS/PMA-treated e-CAS cells in a dose-dependent manner. These results suggest that the antioxidative properties of ketamine in e-CAS cells are most likely related to an indirect, GSH-sparing effect of ketamine.

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