动物造模 z-bio 2021-09-09 424

　　Objective: To observe the effect of emodin on fat browning in apolipoprotein E knockout (ApoE-/ -) mice, and to explore its mechanism of improving blood stasis such as hyperlipidemia.

　　Methods: After 12 weeks of high-fat diet, male 8-week-old ApoE-/- mice were randomly divided into 3 groups, model group, simvastatin 5.7 mg/kg group, emodin 80 mg/kg group; male C57BL/ at the same age 6J mice were the normal control group and were fed with basic feed. The mice in each group were fed with corresponding drugs or drinking water according to the dose for 18 weeks. The detection indicators include bodyweight (BW) and inguinal white adipose tissue (inguinal white adipose tissue). , iWAT) weight, brown adipose tissue (BAT) weight, blood lipids, cardiac function, iWAT pathological features, and in situ expression of uncoupling protein 1 (uncoupling protein UCP1) iWAT.

　　Results: Emodin can significantly reduce mouse body weight (P<0.05), iWAT weight/body weight ratio (P <0.05) and serum TC and TG content (P <0.05), and increase BAT weight/body weight ratio (P <0.05) And cardiac ejection fraction (EF) and fractional shortening (FS) (P <0.01); HE staining results show that iWAT cells appear multi-chambered, the cells become smaller and rounder, and the tissue is more dense ; Immunohistochemistry results showed that the average optical density (AOD) of the positive expression of UCP1 protein in iWAT increased significantly (P <0.01).

　　Conclusion: Emodin can promote the browning of white adipose tissue in the groin of ApoE-/-mice, reduce the accumulation of white fat and improve the symptoms of hyperlipidemia, which may be related to its effect on removing blood stasis.