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A study on regulatory mechanism of miR-223 in ulcerative colitis through PI3K/Akt-mTOR signaling pathway.

Abstract：

OBJECTIVE:The aim of this study was to explore the regulatory mechanism of micro ribonucleic acid (miR)-223 in ulcerative colitis (UC) through the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)-mammalian target of rapamycin (mTOR) signaling pathway. MATERIALS AND METHODS:A total of 36 Sprague-Dawley (SD) rats were randomly divided into three groups, including normal group (n=12), model group (n=12) and inhibitor group (n=12). Rats in the normal group received no treatment. Rats in the model group were used to establish a UC model. Meanwhile, rats in the inhibitor group underwent intraperitoneal injection of inhibitor and establishment of the UC model. Subsequently, specimens were obtained for detection. Immunohistochemistry was applied to measure the expression of mTOR. Western blotting was adopted to determine the relative protein expressions of P85, P110 and phosphorylated Akt (p-Akt). Quantitative polymerase chain reaction (qPCR) was used to detect the mRNA expression of miR-223. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) was utilized to determine cell apoptosis. Furthermore, an enzyme-linked immunosorbent assay (ELISA) was conducted to measure the content of interleukin-1 beta (IL-1β) and IL-6. RESULTS:Immunohistochemistry showed that the positive expression of mTOR increased remarkably in the model group and inhibitor group when compared with that of the normal group (p<0.05). However, it decreased notably in the inhibitor group when compared with the model group (p<0.05). Western blotting indicated that the protein expressions of P85, P110 and p-Akt in model group and inhibitor group were significantly higher than the ones of the normal group (p<0.05). However, the inhibitor group showed markedly lower relative protein expressions of P85, P110 and p-Akt than the ones of the model group (p<0.05). Compared with the normal group, the expression level of miR-223 was significantly elevated in model group and inhibitor group (p<0.05). However, there was no significant difference in the mRNA expression of miR-233 between the model group and the inhibitor group (p>0.05). The apoptosis rate of the cells increased prominently in the model group and in the inhibitor group when compared with the normal group (p<0.05). However, it was remarkably reduced in the inhibitor group than the model group (p<0.05). In comparison with the normal group, the content of IL-1β and IL-6 was significantly up-regulated in the model group and in the inhibitor group (p<0.05). However, it declined notably in the inhibitor group compared with the model group (p<0.05). CONCLUSIONS:MiR-223 can trigger cell apoptosis and inflammation in UC by up-regulating the PI3K/Akt-mTOR signaling pathway.

journal_name

Eur Rev Med Pharmacol Sci

journal_title

European review for medical and pharmacological sciences

authors

Jiang W,Han YP,Hu M,Bao XQ,Yan Y,Chen G

doi

10.26355/eurrev_201906_18074

subject

Has Abstract

pub_date

2019-06-01 00:00:00

pages

4865-4872

issue

eissn

1128-3602

issn

2284-0729

journal_volume

pub_type

杂志文章

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A study on regulatory mechanism of miR-223 in ulcerative colitis through PI3K/Akt-mTOR signaling pathway.