OBJECTIVE To investigate the hypoglycemic effect of Qidan Fang on diabetic mice and explore its relevant mechanism.
METHODS The SPF ICR mice were intraperitoneally injected with 120 mg·kg-1 alloxan after fasting for 16 h. The blood glucose was measured after fasting for 12 h after 5 d. The blood glucose of 10~25 mmol·L-1 was defined as the successful establishment of the diabetic mouse model. The male diabetic ICR mice were divided into the model group, metformin group, low-, medium- and high-dose Qidan Fang groups (0.34, 0.67, 1.34 g·kg-1·d-1, respectively), and administrated for 30 d. Additionally, normal male ICR mice were selected as the blank group. Body mass and fasting blood glucose (FBG) were recorded once every 10 d, and a glucose tolerance test (OGTT) was performed after 30 d. Serum insulin level was detected by ELISA, and then pancreas and liver tissues were collected for HE staining to observe their pathological changes. The expression levels of IRS-1, PI3K, AKT and GLUT4 in the liver tissues were determined by Western blot and qPCR.
RESULTS Compared with the model group, the level of FBG and glucose tolerance decreased significantly (P < 0.01), and the serum insulin level increased significantly (P < 0.01), in the medium- and high-dose Qidan Fang groups; The tissue structure of the pancreas and liver was significantly improved, islet morphology recovered to a certain extent, and liver tissue abnormalities and vascular congestion were rarer in the low-, medium- and high-dose Qidan Fang groups. High dose of Qidan Fang could significantly up-regulate the protein expression levels of p-IRS-1/IRS-1, p-PI3K/PI3K, p-AKT/AKT and GLUT4 in liver tissues (P < 0.01), while significantly up-regulate the mRNA levels of IRS-1, PI3Kp85α, AKT1 and GLUT4 in liver tissues (P < 0.01).
CONCLUSION Qidan Fang has a hypoglycemic effect on diabetic mice, and its mechanism is relative to the regulation of IRS-1/PI3K/AKT signaling pathway.
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