OBJECTIVE: Acute lung injury (ALI) is the most common organ damage in sepsis and sepsis-induced ALI is a clinically extremely dangerous disease. Therefore, it is essential to find an effective way to treat ALI. We hope to provide a new target for the treatment of clinical ALI by studying the effect of GDF11 on LPS-induced ALI. MATERIALS AND METHODS: C57BL/6 male mice and lipopolysaccharide (LPS) were used to induce mouse ALI. Recombinant GDF11 protein was used to treat mice to detect the effect of GDF11 on mouse ALI. In addition, BEAS-2B cells were used to further validate the effects of GDF11 on inflammation and apoptosis of alveolar epithelial cells. RESULTS: Recombinant GDF11 protein significantly reduced the expression of inflammatory factors and apoptosis-related pathways in mouse lung tissues. Overexpression of GDF11 in BEAS-2B cells also significantly attenuated the levels of inflammation and apoptosis in the cells. In addition, GDF11 can reduce the activity of TLR2/HMGB1/NF-κB signaling pathway, which is an important mechanism for GDF11 to play a role in lung protection. CONCLUSIONS: GDF11 can exert lung protection effects by inhibiting the TLR2/HMGB1/NF-κB signaling pathway and reduce the level of inflammation and apoptosis of the lung.
OBJECTIVE: Acute lung injury (ALI) is the most common organ damage in sepsis and sepsis-induced ALI is a clinically extremely dangerous disease. Therefore, it is essential to find an effective way to treat ALI. We hope to provide a new target for the treatment of clinical ALI by studying the effect of GDF11 on LPS-induced ALI. MATERIALS AND METHODS: C57BL/6 male mice and lipopolysaccharide (LPS) were used to induce mouse ALI. Recombinant GDF11 protein was used to treat mice to detect the effect of GDF11 on mouse ALI. In addition, BEAS-2B cells were used to further validate the effects of GDF11 on inflammation and apoptosis of alveolar epithelial cells. RESULTS: Recombinant GDF11 protein significantly reduced the expression of inflammatory factors and apoptosis-related pathways in mouse lung tissues. Overexpression of GDF11 in BEAS-2B cells also significantly attenuated the levels of inflammation and apoptosis in the cells. In addition, GDF11 can reduce the activity of TLR2/HMGB1/NF-κB signaling pathway, which is an important mechanism for GDF11 to play a role in lung protection. CONCLUSIONS:GDF11 can exert lung protection effects by inhibiting the TLR2/HMGB1/NF-κB signaling pathway and reduce the level of inflammation and apoptosis of the lung.