NINL and acute respiratory distress syndrome: In addition, we found that TK-NLP could competitively bind to platelets for inhibiting the formation of PNAs, target and accumulate in the injured lung sites and then respond to the overexpressed ROS to control Nar release, which inhibited the secretion of inflammatory factors, neutrophil infiltration in the lung sites, and protected the integrity of the lung barrier to ameliorate LPS-induced ALI.