Effect of miR-29b on rats with gestational diabetes mellitus by targeting PI3K/Akt signal.

OBJECTIVE

To investigate the role of micro-ribonucleic acid-29b (miR-29b) in rats with gestational diabetes mellitus (GDM) through the phosphatidylinositol 3-kinase (PI3K)/serine/threonine kinase (Akt) signal and its mechanism by establishing rat models of GDM.

MATERIALS AND METHODS

Rat models of GDM were constructed, and then the expression levels of miR-29b, total PI3K, phosphorylated PI3K (p-PI3K), total Akt and phosphorylated Akt (p-Akt) in the model group and control group were measured via Reverse Transcription-Polymerase Chain Reaction (RT-PCR) and Western blotting assays, and the association between miR-29b expression and total PI3K expression was analyzed. In addition, miR-29b mimics and inhibitors were used to further explore the regulatory pathway, and the influences of miR-29b mimics and inhibitors on PI3K and Akt phosphorylation in GDM rats, characteristic indicators of oxidative stress such as superoxide dismutase (SOD), catalase (CAT) and malondialdehyde (MDA) in liver tissues of GDM rats, and fasting blood glucose in GDM rats were studied.

RESULTS

Compared with those in the control group, miR-29b expression was lowered in rat models of GDM, while PI3K/Akt signal expression was increased. In rats with GDM, miR-29b expression was prominently negatively correlated with total PI3K expression (r=-0.777, p=0.007, p<0.01). MiR-29b mimics could reduce PI3K and Akt phosphorylation, increase SOD and CAT expression levels and decrease MDA content (p<0.05). Moreover, miR-29b mimics significantly lowered the blood glucose level in rats with GDM (p<0.05).

CONCLUSIONS

MiR-29b mimics can alleviate oxidative stress and reduce blood glucose by inhibiting the PI3K/Akt signal transduction.