Glucosamine inhibits inflammation in LPS-induced acute lung injury mice

초록

Acute lung injury (ALI) is a common complication of sepsis in patients with impaired immune function. Previous studies have shown that glucosamine inhibits LPS-induced inflammation by inhibiting NF-κB activation in vitro. In this study, we aimed to investigate suppressive effects of glucosamine on the inflammatory response in the lungs of LPS-induced sepsis mice. Mice were intraperitoneally (i.p.) injected with lipopolysaccharide (LPS, 5 mg/kg) to induce sepsis-induced acute lung injury. One group mice were i.p. injected with glucosamine (200 mg/kg) at 2hr before LPS injection. Our data show that glucosamine inhibited LPS-induced nitric oxide (NO) and lactate production in serum as well as attenuated LPS-induced elevation of NO synthase (iNOS) in lung homogenates. Expression of interleukin-1β, interleukin-6 and tumor necrosis factor-α by LPS was inhibited in the glucosamine-pretreated LPS group. In addition, immunohistochemistry and western blot analysis show that glucosamine-pretreated LPS group significantly increased O-GlcNAcylation compared to LPS group. In particular, O-GlcNAcylation of c-Rel, a member of NF-kB, increased in lung homogenates of LPS-induced sepsis mice, while glucosamine attenuated these effects. These results demonstrate that glucosamine inhibits inflammations LPS-induced acute lung injury by inhibiting NF-kB activity.