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SS-31 protects against paraquat-induced lung injury and fibrosis via inhibition of the MAPK signal pathway

ABSTRACT: Aims: To explore the therapeutic effect of SS-31 on lung injury and lung fibrosis caused by paraquat (PQ). Methods: In vivo experiments involved the intraperitoneal injection of PQ solution into C57BL/6 mice to induce lung injury and fibrosis. Subsequently, SS-31 solution was administered intraperitoneally on a daily basis to investigate its protective effects against PQ-induced lung injury and fibrosis. In vitro use of PQ caused inflammatory responses in A549 cell line, and the therapeutic effects of SS-31 were explored by treatment with different concentrations of SS-31 in A549. The SS-31 pathway of action was explored and validated by RNA sequencing. Results: In vivo, SS-31 reduced PQ-induced mortality, acute lung injury, lung fibrosis and apoptosis in mice. The same results were obtained iin vitro experiments. SS-31 was found to inhibit the MAPK pathway by RNA sequencing. The mechanism was further validated by verifying MAPK pathway proteins and applying MAPK pathway agonists. Innovation and Conclusion: In vivo and in vitro experiments demonstrated that SS-31 reduces lung injury and fibrosis induced by PQ. It works through inhibition of the MAPK signaling pathway.

ORGANISM(S): Homo sapiens

PROVIDER: GSE261616 | GEO | 2026/03/15

REPOSITORIES: GEO

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	GSE261616_gene_count.xls.gz	Xls

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Project description:The etiology of trauma-hemorrhage shock-induced acute lung injury has been difficult to elucidate due, at least in part, to the inability of in vivo studies to separate the non-injurious pulmonary effects of trauma-hemorrhage from the tissue injurious ones. To circumvent this in vivo limitation, we utilized a model of trauma-hemorrhagic shock (T/HS) in which T/HS-lung injury was abrogated by dividing the mesenteric lymph duct. In this way, it was possible to separate the pulmonary injurious response from the non-injurious systemic response to T/HS by comparing the pulmonary molecular response of rats subjected to T/HS which did and did not develop lung injury as well as to non-shocked rats. Utilizing high-density oligonucleotide arrays and treatment group comparisons of whole lung tissue collected at 3 hours after the end of the shock or sham-shock period, 139 of the 8,799 assessed genes were differentially expressed. Experiment Overall Design: Four groups of rats (n=3) were studied in order to identify changes in pulmonary gene expression associated with T/HS, both in the presence and absence of lung injury. These included trauma-sham shock (T/SS) rats which had a laparotomy (trauma) but were not subjected to hemorrhagic shock. These rats had no lung injury and served as controls for rats which were subjected to T/HS (laparotomy plus 90 min of shock) and had lung injury. Differences in gene expression between these two groups would represent both the effects of hemorrhagic shock as well as lung injury. To distinguish the gene response of hemorrhagic shock from the gene response associated with lung injury, gene expression was also compared between T/HS rats (hemorrhage and lung injury) and rats subjected to T/HS plus lymph duct ligation (T/HS-LDL), since the T/HS-LDL rats experienced hemorrhagic shock but had no measurable lung injury. Lastly, to identify hemorrhagic shock- modified genes, the pulmonary gene response of T/HS-LDL (hemorrhage without lung injury) were compared to rats subjected to T/SS plus LDL (no hemorrhage or lung injury). Three hours after the end of the 90 min shock or sham-shock period (i.e. 4.5 hrs after the induction of T/HS), the rats were sacrificed and specimens harvested for genechip analysis and histology.

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SS-31 protects against paraquat-induced lung injury and fibrosis via inhibition of the MAPK signal pathway

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