动物造模 z-bio 2021-10-14 409

　　Objective: How to observe the effect of emodin on fat browning in apolipoprotein knockout (ApoE-/-) mice, and explore the mechanism of improving hyperlipidemia and other congestion?

　　Method: 8-week-old male ApoE-/- mice were randomly divided into 3 groups after 12 weeks of high-fat diet. Model group? Simvastatin 5.7 mg/kg group? Emodin 80 mg/kg group; male C57BL/6J mice of the same age in the normal control group and basic diet. According to the dose, each group of mice received the corresponding drugs or drinking water for 18 weeks. The test indicators are body weight (BW) and the weight of inguinal white adipose tissue (inguinal white adipose tissue, iWAT)? Contains brown fat. The weight of the organization (BAT)? Blood lipids? Cardiac Function? Pathological characteristics of iWAT and uncoupling protein 1 (Uncoupling protein UCP1) iWAT in situ expression?

　　Result: Can emodin significantly reduce the weight of mice (P\u003c0.05)? iWAT weight/weight ratio (P\u003c0.05) and serum TC? Did TG content (P\u003c0.05), BAT weight/weight ratio (P\u003c0.05) and cardiac ejection fraction (excretion fraction, EF) increase? Short axis shortening rate (partial shortening), FS) (P\u003c0.01); HE staining results show that iWAT cells appear multi-cavity, the cells are small and round, and the tissue is denser. The results of immunohistochemistry showed that the positive expression of UCP1 protein in iWAT was average. Is the optical density (average optical density, AOD) significantly improved (P\u003c0.01)?

　　Conclusion: Emodin can promote the browning of the white adipose tissue of ApoE-/- mice, reduce the accumulation of white fat and improve symptoms. It is related to the elimination of hyperlipidemia and congestion. What is your possible role?