Abstract
Objective To explore the protective effect of GAS6 (growth arrest-specific gene 6 protein) on lung injury in septic mice so as to elucidate the mechanism. Methods Ninty male BALB/c mice were divided into 6 groups (n=15): sham operation group, CLP group, CLP+ vehicle group, CLP+ GAS6 group (1 μg), CLP+ GAS6 group (5 μg), CLP+ GAS6 group (10 μg). Mice in CLP groups and GAS6 groups were made to be sepsis models by CLP. GAS6 was administrated after CLP in GAS6 groups by intravenous injection. And mice in sham group were only treated with laparotomy without CLP. And 24 h later, all survived mice were sacrificed to obtain blood and lung tissue. Serum levels of TNF-α, IL-1β were measured by using ELISA. The lung wet/dry ratio was calculated. Histopathological changes of lung tissues were observed under light microscope. NF-κB and IκB-α were assayed by Western blotting. Data were analyzed by SPSS 23.0. Statistical analyses were performed using independent sample t-test to compare between two groups or one-way analysis of variance test to compare among multiple groups. Results The serum levels of TNF-α (P=0.000), IL-1β (P=0.000), the lung W/D (P=0.000), pulmonary pathological change (P=0.000), the levels of NF-κB(P=0.006) in CLP group were higher than those in sham group, while IκB-α (P=0.001) in CLP groups was lower than those in sham group. The GAS6 significantly reduced the serum levels of TNF-α (P=0.000), IL-1β (P=0.000), the lung W/D (P=0.000), pathogenesis of lung tissue (P=0.000) and the levels of NF-κB (P=0.000) in septic mice. The IκB-α (P=0.009)was increased after treatment with GAS6 in a dose-dependent manner. Conclusions GAS6 has protective effect on septic lung injury in mice, and its molecular mechanism may be associated with inhibiting inflammatory response and suppressing NF-κB nuclear translocation. Key words: Gas6; Sepsis; Mice; Acute lung injury; Inflammatory factors; TNF-α; IL-1β; NF-κB; IκB-α
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