Gelsolin Attenuates Lipopolysaccharide-Induced Acute Lung Injury in Rats by Modulating TLR4/Myd88/NF-κB Signaling Pathway

Hai-Yan Fu, Zhan-Sheng Hu, Xiao-Ting Dong, Rong-Bin Zhou and Hong-Yang Du

Background and Objective: Gelsolin (GSN) is an important actin protein that can bind to actin and regulate the polymerization and depolymerization of actin. It is closely related to apoptosis, coagulation, immunity, tumour and inflammation. This study aimed to investigate the intervention effects and mechanism of GSN on LPS-induced ALI in rats. Materials and Methods: GSN of different concentrations (0.1, 0.3, 0.9 mg kg^–1) were used to treat LPS-induced ALI rats. Pathological changes of lung tissue and the contents of TNF-α, IL-6 and IL-1β in BALF, serum and lung tissue homogenate were measured by ELISA. The expressions of TLR4, MyD88, IRAK1, TRAF6, TAK1, IκBα and NF-κB p65 in lung tissue were detected at protein and gene levels by western blot and qRT-PCR. Results: The results showed that GSN markedly attenuated the histological alterations and suppressed the levels of TNF-α, IL-6 and IL-1β in BALF, serum and lung tissue homogenate. Furthermore, the expression of TLR4, MyD88, IRAK1, TRAF6, TAK1 and NF-κB p65 induced by LPS were markedly inhibited by GSN and the expression of IκBα increased at protein and gene levels. Conclusion: This study demonstrated that GSN attenuated LPS-induced acute lung injury in rats by modulating TLR4/MyD88/NF-κB signalling pathway.

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