AC2-26 alleviates cardiopulmonary bypass serum-induced injury via ERK/NF-κB pathway in rat alveolar type Ⅱ epithelial cells
Objective To investigate the effect and mechanism of membrane associated protein A1 peptide AC2-26 on serum induced alveolar type Ⅱ epithelial cell injury in rats during cardiopulmonary bypass(CPB).Meth-ods Sixteenpatients undergoing rheumatic heart disease surgery were included,and sterile blood was collected and serum was separated after CPB shutdown.Primary alveolar type Ⅱ epithelial cells were extractedfrom healthy rats,cultured for 72 h,and then randomly divided into five groups:control group(groupC),alveolar type Ⅱepithelial cell(AEC Ⅱ)injury group(groupM),AC2-26+AEC Ⅱ injury group(groupA),AEC Ⅱ injury+Boc2 group(groupB),and AC2-26+AEC Ⅱ injury+Boc2 group(groupA+B).CCK-8and flow cytometry was used to detect the proliferation and apoptosis of cells in each group;Immunofluorescence was used to detect formyl peptide receptor 2(FPR2)and pulmonary surfactant(SPC)expression in type Ⅱ alveolar epithelial cells of each group;The alveolar type Ⅱ epithelial cell lamellar bodies were observed using transmission electron mi-croscopy;Western blot was used to detect the expression of ERK and NF-κB in alveolar type Ⅱ epithelial cells of each group.Results After the application of AC2-26,the proliferation rate of alveolar type Ⅱ epithelial cells induced by CPB serum significantly increased,and the apoptosis rate significantly decreased(P＜0.05).AC2-26 significantly inhibited the phosphorylation of ERK and NF-κ B proteins(P＜0.05),promoted the expression of SPC,and improved the structure and morphology of intracellular lamellar bodies.This phenomenon can be blocked by the formyl peptide receptor inhibitor Boc2.Conclusion AC2-26 can alleviate CPB serum induced damage to alveolar type Ⅱ epithelial cells,and its mechanism of action may be related to FPR2 regulating the ERK and NF-κB signaling pathways.
annexin A1alveolar type Ⅱ epithelial cellscardiopulmonary bypasslung injury
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