Purpose: Do you want to observe the effect of emodin on fat browning in apolipoprotein knockout (ApoE-/-) mice, and explore the mechanism of improving congestion such as hyperlipidemia?
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 were in the normal control group, and each group of mice was provided with corresponding drugs or drinking water for 18 weeks according to the dose. The test indicators include the body weight (BW) and body weight of the inguinal white adipose tissue (inguinal white adipose tissue, iWAT). Adipose tissue (BAT) weight? Blood lipids? Cardiac Function? The pathological characteristics of iWAT and protein 1 isolation (protein UCP1 isolation) iWAT expression in situ?
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 (fraction shortening, FS) (P\u003c0.01); HE staining results show that iWAT cells are multi-lumen, cells are small and round, and tissues are denser. The results of immunohistochemistry showed that the positive expression of UCP1 protein in iWAT significantly increased the average optical density (average optical density, AOD) (P\u003c0.01)?
Conclusion: Emodin promotes the browning of the white adipose tissue of the ApoE-/- mice and reduces the accumulation of white fat in the symptoms of hyperlipidemia, which is related to the elimination of congestion.