PURPOSE: Ghrelin possesses anti-inflammation effect on rat model of cardiovascular disease and arthritis. It also inhibits the expression of pro-inflammatory cytokines in some cells. In the lung, both ghrelin and its receptor expressed in a variety of cells. This broad expression suggests that ghrelin may function as signal modulators in the lung. However, whether ghrelin has anti-inflammatory effect in acute lung injury remains unknown.
METHODS: Acute lung injury was induced by intratracheal instillation of LPS in rats. Lung injury was assessed by histological examination. Lung macrophage was isolated and incubated with LPS, N-omega-Nitro-L-arginine methyl ester (L-NAME) and ghrelin. TNF-alpha and IL-1 beta concentrations in BAL fluid and culture supernatant were determined by ELISA. Nitric oxide (NO) in BAL fluid and culture supernatant, NO synthase (NOS) in culture macrophage were detected by a spectrophotometric measurement method.
RESULTS: hrelin attenuated LPS-induced acute lung injury, inhibited the production of pro-inflammatory cytokines and increased the NO concentration in BAL fluid. Ghrelin also suppressed the LPS-induced expression of pro-inflammatory cytokines, increased NOS activity in cultured macrophage and NO concentration in culture supernatants. However, this anti-inflammation effect of ghrelin was inhibited by L-NAME.
CONCLUSION: Ghrelin attenuates LPS-induced acute lung inflammation in rats and suppresses LPS-induced pro-inflammatory cytokines production in cultured lung macrophage. Furthermore, the anti-inflammatory effect of Ghrelin may be mediated by increasing NO production.
CLINICAL IMPLICATIONS: Ghrelin may be used in ALI for attenuating the inflammation in the lung.
DISCLOSURE: FengMing Luo, None.