Propofol Potentiates Sevoflurane-Induced Inhibition of Nuclear Factor--κB-Mediated Inflammatory Responses and Regulation of Mitogen-Activated Protein Kinases Pathways via Toll-like Receptor 4 Signaling in Lipopolysaccharide-Induced Acute Lung Injury in Mice

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Abstract

Background:

Toll-like receptor 4 (TLR4)-induced initiation of mitogen-activated protein kinases and the nuclear factor-kappa B signaling cascade is reportedly involved in inflammatory responses during lung injury. Studies have found that volatile anesthetics, such as isoflurane and sevoflurane, inhibit inflammation. This investigation explored the protective effects of propofol and whether propofol potentiates the protective effects of sevoflurane against lipopolysaccharide (LPS)-induced acute lung injury.

Materials and Methods:

Male BALB/c mice were treated with LPS (10 μg/mouse; intranasal instillation) to induce acute lung injury. Mice were exposed to sevoflurane (3%; 6 hours) alone or combined with propofol (10 or 20 mg/kg body weight; subcutaneously) followed by sevoflurane for 1 hour before the LPS challenge.

Results:

Sevoflurane with or without propofol attenuated pulmonary edema, restored altered lung architecture and reduced influx of inflammatory cells into bronchoalveolar lavage fluid after the LPS challenge. LPS-mediated overproduction of the proinflammatory cytokines tumor necrosis factor-α, interleukin-1β, and interleukin-6 as well as nitric oxide, were reduced. Sevoflurane either alone or with propofol downregulated TLR4 and TLR4-mediated mitogen-activated protein kinase and nuclear factor-kappa B signaling.

Conclusions:

Combined exposure to propofol and sevoflurane was more effective than sevoflurane administered alone, suggesting the positive effects of propofol on sevoflurane-mediated anti-inflammatory effects.

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