Herb-partitioned moxibustion regulated the miRNA expression pro-file in the thyroid tissues of rats with experimental autoimmune thy-roiditis
摘要OBJECTIVE:To observe the effect of herb-parti-tioned moxibustion (HPM) on the miRNA expres-sion profile of thyroid tissue in experimental auto-immune thyroiditis (EAT) rats.METHODS:Rats were randomly divided into nor-mal control (NC) group,EAT model (EAT) group,HPM group and western medicine (Med) group.EAT model rats were prepared by a combined im-munization with complete and incomplete Freund's adjuvant emulsified with porcine thyro-globulin and iodine.Rats in the HPM group were treated with HPM,while rats in the Med group were treated with levothyrocine (1 μg/2 mL) by ga-vage.HE staining was used to observe the patho-logical morphological changes of thyroid tissue,ELISAs was uaed to detect the serum concentra-tions of TGAb,TPOAb,FT3,FT4,TSH.We then per-formed high-throughput miRNA sequencing to analyse the miRNA expression profiles in the thy-roid tissues,followed by a bioinformatics analysis.RT-qPCR was used to verify the identified differen-tially expressed miRNAs.RESULTS:HPM improved the thyroid tissue mor-phology and reduced serum TPOAb,TGAb,TSH con-centration in EAT rats (P < 0.05),but with no obvi-ous effect on FT3 and FT4 concentration.While the TSH,FT3 and FT4 concentration was significantly changed in the Med group (P < 0.01 or P < 0.05)compared with that of EAT group.Sequencing re-sults showed that a total of 17 miRNAs were upreg-ulated,and 4 were downregulated in the EAT rats,in which the expression levels of miR-346 and miR-331-5p were reversed by HPM.The target genes of the miRNAs that regulated by HPM were associated with a variety of immune factors and im-mune signals.RT-qPCR verification showed that the expression of miRNA-346 and miRNA-331-5p was consistent with the sequencing results.CONCLUSIONS:HPM could regulate the the ex-pression of miRNA-346 and miRNA-331-5p,then act on their target genes to immune and inflamma-tion-related pathways,which may be one of the mechanisms of HPM on EAT rats.
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