Protective effects of notoginsenoside R1 on acute lung injury in rats with sepsis

Background To clarify the mechanism of notoginsenoside R1 in the treatment of septic acute lung injury (ALI) based on network pharmacological analysis, and to verify it in the model of septic ALI in rats. Methods Based on database searching, the related targets of notoginsenoside R1 and ALI were identified, and the component-disease-target network was constructed. The core targets were screened by protein-protein interaction (PPI), and the functional enrichment of Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) was analyzed. The rat model of septic ALI was further established to investigate the pharmacological effects of notoginsenoside R1. Results Notoginsenoside R1 possibly affected ALI through 150 targets, of which 36 were core targets. GO semantic similarity analysis showed that notoginsenoside R1 might play a role in regulating interleukin 17 (IL-17) signal pathway, tumor necrosis factor (TNF) signal pathway and other key links by regulating MAPK1, MAPK3, IL-1β and other targets. The results of pharmacological experiments showed that notoginsenoside R1 could significantly reduce the wet:dry ratio of the lung in an animal model of ALI, improve the pathological injury of the lung, and reduce the content of IL-1β in serum and in bronchoalveolar lavage fluid (BALF) of experimental animals. Conclusions Notoginsenoside R1 can inhibit pulmonary edema, reduce inflammation, and improve lung lesions through multiple targets and pathways to achieve the pharmacological effects in the treatment of septic ALI.