Doxycycline reduces mortality to lethal endotoxemia by reducing nitric oxide synthesis via an interleukin-10-independent mechanism.
basic_science · Level V
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Abstract
It was demonstrated that doxycycline protected BALB/c mice injected intraperitoneally with bacterial lipopolysaccharide (LPS) against lethal septic shock. Doxycycline (at 1.5 mg/kg) exerted its protective effect by inhibiting nitrate production by an interleukin-10-independent mechanism. Experiments carried out in vitro also indicated that doxycycline inhibited NO synthesis by LPS-activated macrophages without inducing any significant modification in interleukin-10 release. These data suggest that the direct inhibition of nitrate release is the main mechanism of the antiinflammatory activity of doxycycline in septic shock.
Medical subject headings
- Anti-Bacterial Agents
- Doxycycline
- Endotoxemia
- Interleukin-10
- Nitric Oxide