在老鼠为 hyperlipidemia 的处理调查效果和 8-hydroxy dihydroberberine (Hdber ) 的不同剂量的分子的机制。
Objective: To investigate the effect and molecular mechanisms of different doses of 8-hydroxy dihydroberberine (Hdber) for the treatment of hyperlipidemia in rats. Methods: A rat model of hyperlipidemia was established by feeding rats a high-fat diet for 4 weeks in 70 rats of 80 animals, and 10 rats were randomly selected as control group. The hyperlipidemic rats were then randomly divided into the following groups: a model group (MOD); a berberine group [BBR, 156 mg/(kg.day)]; Hdber groups, which were treated with different doses of Hdber [78, 39 and 19.5 mg/(kg.day)]; and a simvastatin group [SIM, 4 mg/(kg.day)]. The corresponding therapy was administered to the rats of each treatment via gastric tubes. Normal animals were used as a control group. The blood levels of various lipids, including total cholesterol, triglycarides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, free fatty acid (FFA), apolipoprotein A I (Apo-A I ) and apolipoprotein B (APO-B) were examined. The protein expressions of low-density lipoprotein receptor (LDL-R), sterol regulatory element-binding protein 2 (SREBP-2), 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) and proprotein convertase subtilisin/kexin type 9 (PCSK-9) in liver tissues were determined by Western blot analysis. Results: Compared with the control group of rats, the model group demonstrated a deteriorated blood lipid profile and exhibited increased expression levels of PCSK-9 protein in their liver tissues (P〈0.01). In addition, the high-fat diet decreased the expression levels of LDL-R, SREBP-2 and HMGCR proteins in murine liver tissues. However, the addition of berberine or Hdber reversed the blood lipid profile changes (P〈0.05 or P〈0.01), decreased the expression levels of PCSK-9 proteins (P〈0.01), and increased the expression levels of LDL-R proteins in the hyperlipidemic rats (P〈0.01). These compounds did not significantly influence the expression leve