Effect of emodin on long non-coding RNA-mRNA networks in rats with severe acute pancreatitis-induced acute lung injury

ABSTRACT: Long non-coding RNAs (lncRNAs) reportedly contribute to disease pathogenesis and drug treatment effects. Both emodin and dexamethasone (DEX) have been used for the treatment of severe acute pancreatitis-associated acute lung injury (SAP-ALI). However, lncRNA regulation networks related to SAP-ALI pathogenesis and drug treatment are unreported. In this study, lncRNAs and mRNAs in the lung tissue of SAP-ALI and control rats, with or without drug treatment (emodin or DEX), were assessed by RNA sequencing. Results showed that both emodin and DEX were therapeutic for SAP-ALI and that mRNA and lncRNA levels differed between untreated and treated SAP-ALI rats. Gene expression profile relationships for emodin treated and control rats were higher than DEX treated and untreated animals. By comparison of control and SAP-ALI animals, more upregulated than downregulated mRNAs and lncRNAs were observed with emodin treatment. For DEX treatment, more downregulated than upregulated mRNAs and lncRNAs were observed. Functional analysis demonstrated both upregulated mRNA and co-expressed genes with upregulated lncRNAs were enriched in inflammatory and immune response pathways. Further, emodin associated lncRNAs and mRNAs co-expressed modules were different from those associated with DEX. Quantitative polymerase chain reaction demonstrates that selected lncRNA and mRNA co-expressed modules were different in the lung tissue of emodin and DEX treated rats. Also, emodin had different effects compared to DEX on the co-expression network of lncRNAs Rn60_7_1164.1 and AABR07062477.2 for the blue lncRNA module and Nrp1 for the green mRNA module. In conclusion, this study provides evidence that emodin may be a suitable alternative or complementary medicine for treatment of SAP-ALI.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE151572 | GEO | 2021/01/03

REPOSITORIES: GEO