[Lipid-lowering effect of propolis in mice with Triton-WR1339-induced hyperlipidemia and its mechanism for regulating lipid metabolism]

蜂胶对Triton-WR1339所致高脂血症小鼠的降脂作用及其调节脂代谢的机制研究

阅读:9
作者:Xiaoqi Huang, Xiaoli Wu, Sishan Yan, Tian Lan

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。

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.

Objective

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

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。

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。