Objective To investigate whether long non-coding RNA(lncRNA)myocardial infarct-associat-ed transcription factor(MIAT)promotes sepsis-induced acute kidney injury(AKI)by regulating microRNA-338-3p(miR-338-3p)/platelet thromboplastin-1(THBS1)axis.Methods Septic AKI model was established by cecal ligation and puncture.The rats were divided into control group and sepsis AKI group,with 10 rats in each group.The expression levels of lncRNA MIAT,miR-338-3p and THBS1gene in renal tissue were detec-ted by quantitative real-time PCR(qPCR).The levels of serum urea nitrogen(BUN)and creatinine(Cre)were detected by automatic biochemical analyzer.Renal tubular epithelial NRK-52E cells were induced by li-popolysaccharide(LPS)to establish a cell model of sepsis induced AKI.NRK-52E cells were divided into CK group,LPS group,LPS+si-NC group,LPS+si-lncRNA MIAT group,LPS+si-lncRNA MIAT+inhibitor NC group,LPS+si-lncRNA MIAT+miR-338-3p inhibitor group,LPS+si-lncRNA MIAT+oe-NC group,LPS+si-lncRNA MIAT+oe-THBS1 group.qPCR was used to detect the expression levels of lncRNA MIAT,miR-338-3p and THBS1 gene in each group.Cell counting kit 8 was used to detect cell proliferation in each group.Flow cytometry was used to detect the apoptosis rate of each group.Enzyme-linked immunosorbent assay was used to detect the levels of lactate dehydrogenase(LDH),tumor necrosis factor-α(TNF-α),interleukin(IL)-6,IL-10,malondialdehyde(MDA)and the activities of superoxide dismutase(SOD)and catalase(CAT)in each group.The expression of NOD-like receptor pyrin domain-containing protein 3(NLRP3),Caspase-1,cleaved caspase-3 and THBS1 protein were detected by Western blot.The targeting relationship between miR-338-3p and lncRNA MIAT and THBS1 was verified.Results The expression levels of BUN,Cre,lncRNA MI-AT and THBS1 gene were increased(P<0.05),and the expression level of miR-338-3p was decreased in sep-sis AKI group(P<0.05).Compared with CK group,the expression of lncRNA MIAT,THBS1 gene,apopto-sis rate and the levels of IL-6,LDH,TNF-αand MDA were significantly increased(P<0.05),the protein ex-pression levels of NLRP3,Caspase-1,cleaved caspase-3 and THBS1 were significantly increased(P<0.05),while the expression of miR-338-3p,A450(24,48 h)value and IL-10 level were significantly decreased(P<0.05),and the activities of CAT and SOD were significantly decreased in LPS group and LPS+si-NC group(P<0.05).Compared with LPS+si-NC group,the expression of lncRNA MIAT,THBS1 gene,apoptosis rate and the levels of IL-6,LDH,TNF-α and MDA were significantly decreased(P<0.05),the protein expression levels of NLRP3,Caspase-1,cleaved caspase-3 and THBS1 were significantly decreased(P<0.05),while the expression of miR-338-3p,A450(24,48 h)value and IL-10 level were significantly increased(P<0.05),and the CAT and SOD activities were significantly increased in LPS+si-lncRNA MIAT group(P<0.05).Silen-cing miR-338-3p expression or up-regulation of THBS1 gene expression could attenuate the improvement effect of lncRNA MIAT on sepsis AKI(P<0.05).Conclusion lncRNA MIAT promotes sepsis-induced AKI through regulating miR-338-3p/THBS1 axis.