Objective: To evaluate the therapeutic effect of propolis against Triton-WR1339-induced hyperlipidemia in mice and explore the underlying mechanism.
Methods: C57BL/6 mice were randomly divided into 7 groups (n=10), including the control group, hyperlipidemia model group, fenofibrate (30 mg/kg) treatment group, and 4 treatment groups treated with low- (30 mg/kg) or high-dose (60 mg/kg) propolis HB01 or HB02. In all but the control group, acute hyperlipidemia models were established by intramuscular injection of Triton WR-1339, and corresponding treatments were administered via gastric lavage for 7 days. After the treatments, blood samples were collected for testing the levels of total cholesterol (TC), triglycerides (TG), highdensity lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C), malondialdehyde (MDA), superoxide dismutase (SOD), alanine aminotransferase (GPT), and aspartate aminotransferase (GOT); Western blotting was used to detect the expressions of the proteins involved in lipid metabolism in the liver tissues including ABCA1, ABCG8, LDLR, and SR-B1.
Results: Compared with the normal control group, the mice with Triton-WR1339-induced hyperlipidemia showed significantly increased levels of TC, TG, LDL, MDA, GPT, and GOT and lowered HDL-C levels and SOD activity (P < 0.05). Treatments with fenofibrate and the 2 propolis at either low or high dose significantly reversed Triton-WR1339-induced changes in blood lipids (P < 0.05), and the effects of propolis were more potent. Triton-WR1339 injection also significantly decreased the expressions levels of ABCA1, ABCG8, LDLR, and SR-B1 in the liver (P < 0.05), and these changes were obviously reversed by treatments with fenofibrate and propolis (P < 0.05), especially by the latter.
Conclusions: The lipid-lowering effects of propolis are mediated by improving lipid metabolism and regulating the expressions of lipid transport proteins in the liver tissue.
目的: 探究蜂胶对Triton-WR1339所致高脂血症的降脂作用及调控脂质代谢机制。
方法: 将C57BL/6小鼠随机分为7组，10只/组，雌雄各半，分别为正常组、模型组、非诺贝特组(30 mg/kg)、蜂胶HB01高剂量组(60 mg/kg)、蜂胶HB01低剂量组(30 mg/kg)、蜂胶HB02高剂量组(60 mg/kg)和蜂胶HB02低剂量组(30 mg/kg)。采用肌肉注射Triton WR-1339试剂造成高脂血症模型，灌胃1周后眼眶取血，离心后测定血清中总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL)、低密度脂蛋白胆固醇(LDL)、丙二醛(MDA)、总超氧化物歧化酶(SOD)、谷丙转氨酶(GPT)、谷草转氨酶(GOT)等指标；取肝脏组织，置-80 ℃保存，Western blot法测定脂质转运蛋白的表达水平。
结果: 与正常组相比，模型组血清中TC、TG、LDL、MDA、GPT、GOT的含量升高，HDL含量降低、SOD活力下降(P < 0.05)。与模型组比较，阳性药(非诺贝特：30 mg/kg)和两种蜂胶(高剂量组：60 mg/kg；低剂量组：30 mg/kg)都能明显降低TC、TG、LDL、MDA、GPT、GOT含量而升高HDL含量，促进SOD活力，差异有统计学意义(P < 0.05)，且蜂胶的效果略优于阳性药组。与正常组相比，Triton-WR1339诱导的模型组肝脏中的ABCA1、ABCG8、低密度脂蛋白和SR-B1等脂质转运蛋白显著下降，差异有统计学意义(P < 0.05)，但阳性药(非诺贝特：30 mg/kg)和蜂胶(高剂量组：60 mg/kg；低剂量组：30 mg/kg)干预后均能逆转这一下降趋势，蜂胶组的干预效果略优于阳性药组，差异有统计学意义(P < 0.05)。
结论: 蜂胶具有显著的降血脂作用，其作用机制与改善肝脏脂质代谢紊乱、调控脂质代谢转运蛋白相关。
Keywords: Triton-WR1339; hypolipidemia; lipid metabolism; propolis.