Apoptosis and surfactant protein-C expression inhibition induced by lipopolysaccharide in AEC II cell may associate with NF-kappa B pathway

作者：Lin, Jinle; Tian, Jun; Wang, Li; Wu, Weigang; Li, Huaying; Wang, Xueyan; Zeng, Xiaobin^*; Zhang, Wenwu^*

来源：Journal of Toxicological Sciences, 2017, 42(1): 53-61.

DOI：10.2131/jts.42.53

• Acute respiratory distress syndrome (ARDS)
• Lipopolysaccharide
• NF-kappa B pathway
• Apoptosis
• Surfactant Protein-C

Lipopolysaccharide (LPS), a Gram-negative bacterial outer membrane component, is one of the major causes of septic shock. Herein we investigate LPS-induced apoptosis of rat alveolar epithelial type II cells (AEC II) and the effects of LPS on surfactant protein-C (SP-C) expression in AEC II, along with the possible molecular mechanisms. LPS exposure impaired cell viability and increased apoptosis of AEC II significantly in concentration-dependent manner embodied in increased caspase-3 expression and the activity of caspase-3. Simultaneously, our results also indicated that LPS inhibited surfactant protein-C (SP-C) expression in AEC II. Mechanistic studies revealed that LPS treatment significantly increased the expression of NF-kappa B p50, NF-kappa B p65 and IKK beta proteins as well as induced I kappa B-alpha phosphorylation. Moreover, pretreatment with IKK inhibitor IKK-16 or NF-kappa B inhibitor PDTC ameliorated LPS-caused alterations in cleaved caspase-3 expression, the activity of caspase-3 and SP-C expression. Taken together, these results demonstrate that LPS can induce apoptosis of AEC II and decrease SP-C expression partly through activating the NF-kappa B pathway.

• 出版日期2017-2
• 单位深圳清华大学研究院; 南方医科大学; 暨南大学