OBJECTIVETo evaluate the therapeutic effect of propolis against Triton-WR1339-induced hyperlipidemia in mice and explore the underlying mechanism.

METHODSC57BL/6 mice were randomly divided into 7 groups (=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.

RESULTSCompared 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 ( < 0.05). Treatments with fenofibrate and the 2 propolis at either low or high dose significantly reversed Triton-WR1339-induced changes in blood lipids ( < 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 ( < 0.05), and these changes were obviously reversed by treatments with fenofibrate and propolis ( < 0.05), especially by the latter.

CONCLUSIONSThe lipid-lowering effects of propolis are mediated by improving lipid metabolism and regulating the expressions of lipid transport proteins in the liver tissue.