动物造模,基因敲除 z-bio 2022-03-28 295

　　Objective: To observe the effect of emodin on fat browning in apolipoprotein E knockout mice, so as to explore its mechanism of improving blood stasis states 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, and emodin 80 mg/kg group; male C57BL/ 6J mice were used as normal control group and were fed with basal diet. Mice in each group were given corresponding drugs or drinking water for 18 weeks of intervention. The detection indicators included body weight (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 iWAT in situ expression of uncoupling protein UCP1.

　　Results: Emodin could significantly reduce the body weight of mice (P < 0.05), iWAT weight/body weight ratio (P < 0.05), 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 showed that iWAT cells appeared multi-chambered, cells became smaller, rounder, and the tissue was more dense ; Immunohistochemical results showed that the average optical density (AOD) of positive UCP1 protein expression in iWAT was significantly increased (P < 0.01).

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