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) contribute to disease pathogenesis and drug treatment effects. Both emodin and dexamethasone (DEX) have been used for treating 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 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 up‐regulated than down‐regulated mRNAs and lncRNAs were observed with emodin treatment. For DEX treatment, more down‐regulated than up‐regulated mRNAs and lncRNAs were observed. Functional analysis demonstrated both up‐regulated mRNA and co‐expressed genes with up‐regulated 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 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 with DEX on 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 treating SAP‐ALI.