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Abstract: Poster Presentations |

GHRELIN ATTENUATES LPS-INDUCED ACUTE LUNG INJURY VIA A MECHANISM THAT INVOLVES THE NO PATHWAY FREE TO VIEW

Xiaojing Liu, PhD; FengMing Luo, MD*
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West China Hospital of Sichuan University, Chengdu, Peoples Rep of China



Chest. 2006;130(4_MeetingAbstracts):209S. doi:10.1378/chest.130.4_MeetingAbstracts.209S-c
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Abstract

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.

Wednesday, October 25, 2006

12:30 PM - 2:00 PM


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