【Objective】 To observe the effects of in vitro exogenous administration of ghrelin on LPS induced apoptosis in rat alveolar macrophage NR8383

and to investigate the potential role of JNK signaling pathway in this impact. 【Methods】 CCK-8 assay was used to examine the cell viability of NR8383 treated by LPS alone or co-incubated by ghrelin and LPS; flow cytometry and TUNEL were used to assessed the apoptosis rate; expression of JNK

phospho-JNK

Bax

Bcl-2

cleaved caspase-3 were detected using Western blot analysis. Laser scanning confocal microscopy was used to observe the phagocytosis of NR8383. Ghrelin receptor antagonist [D-Lys-3]-GHRP-6 and JNK specific inhibitor SP600125 were used to inhibit ghrelin receptor and JNK activation respectively. 【Results】 LPS significantly inhibited the proliferation of NR8383 in a dose-dependent manner

with IC50 value of 250 μg/mL. However

ghrelin can block this inhibition casused by LPS. Flow cytometry and TUNEL analysis showed that ghrelin could decrease the apoptosis induced by LPS in NR8383 (P < 0.05)

while application of ghrelin receptor antagonist [D-Lys-3]-GHRP-6 weakened the antiapoptosis effect of ghrelin(P < 0.05). LPS activated JNK kinase

increased the expression of Bax and cleaved caspase-3

but decreased Bcl-2 level

which was significantly reversed by pretreatment with ghrelin(P < 0.05). Ghrelin also apparently maintained the phagocytosis of NR8383 post LPS treatment (P < 0.05). 【Conclusion】 Ghrelin inhibited LPS induced NR8383 apoptosis by down-regulating JNK signal pathway

and maintained the phagocytosis of NR8383.