摘要：
Sevoflurane, a widely used inhalation anesthetic, has been shown to be cardioprotective in individuals with sepsis and myocardial dysfunction. However, the exact mechanism has not been completely explained. In this study, we performed whole-transcriptome profile analysis in the myocardium of Lipopolysaccharide (LPS) induced septic mice after sevoflurane pretreatment. RNA transcriptome sequencing showed that 97 Protein coding RNAs(mRNAs), 64 long non-coding RNAs (lncRNAs), and 27 microRNAs (miRNAs) were differentially expressed between the LPS and S_L groups. Functional enrichment analysis revealed that target genes for the differentially expressed mRNAs (DE mRNAs) between the two groups participated in Protein processing in the endoplasmic reticulum, Antigen processing and presentation, and the mitogen-activated protein kinase (MAPK) signaling pathway. Bioinformatics study of DE mRNAs revealed that 13 key genes including Hsph1, Otud1, Manf, Gbp2b, Stip1, Gbp3, Hspa1b, Aff3, Med12, Kdm4a, Gatad1, Cdkn1a, and Ppp1r16b are related to heart or inflammation. Furthermore, the Competing endogenous RNA (ceRNA) network revealed that 3 of the 13 key genes established the lncRNA-miRNA-mRNA network (ENSMUST00000192774 --- mmu-miR-7a-5p --- Hspa1b, TCONS_00188587 --- mmu-miR-204-3p --- Aff3 and ENSMUST00000138273 --- mmu-miR-1954 --- Ppp1r16b) may be associated with cardioprotection in septic mice. In general, the findings identified 11 potential essential genes (Hsph1, Otud1, Manf, Gbp2b, Stip1, Gbp3, Hspa1b, Aff3, Med12, Kdm4a, Gatad1, Cdkn1a, and Ppp1r16b) and MAPK signaling pathway involved in sevoflurane-induced cardioprotection in septic mice, In particular, sevoflurane may prevent myocardial injury by regulating the lncRNA-miRNA-mRNA network including (ENSMUST00000192774 - mmu-miR-7a-5p - Hspa1b, TCONS_00188587 - mmu-miR-204-3p - Aff3, and ENSMUST00000138273 - mmu-miR-1954 - Ppp1r16b networks) which may be a novel mechanism of sevoflurane-induced cardioprotection.Copyright © 2022 Wolters Kluwer Health, Inc. All rights reserved.
