FOOD SCIENCE ›› 2018, Vol. 39 ›› Issue (5): 213-219.doi: 10.7506/spkx1002-6630-201805032

• Nutrition & Hygiene • Previous Articles     Next Articles

Protective Effect of Berberine on Oleic Acid-Induced Injury in Human Aortic Endothelial Cells via AMPK-eNOS Activation

ZHOU Hui1,2, LIU Jing1, HOU Wenfeng1, WANG Yaoqing1, ZHANG Wenyan1, XU Bo1, MA Chengjun1, LI Ji1, MENG Qingguo3, SUN Xiling4, WANG Zhenhua1,*   

  1. 1. Center for Mitochondria and Healthy Aging, College of Life Sciences, Yantai University, Yantai 264005, China; 2. Key Laboratory of Xinjiang Endemic Phytomedicine Resources, Ministry of Education, School of Pharmacy, Shihezi University, Shihezi 832002, China; 3. Key Laboratory of Molecular Pharmacology and Drug Evaluation, Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai 264005, China; 4. Shandong Province Key Laboratory of TCM Syndrome, Binzhou Medical University, Yantai 264003, China
  • Online:2018-03-15 Published:2018-03-14

Abstract: Objective: To investigate the protective effect and underlying mechanism of berberine chloride on oleic acid (OA)-induced damage in human aortic endothelial cells (HAECs). Methods: HAECs were treated with oleic acid alone or in combination with berberine, adenosine monophosphate-activated protein kinase (AMPK) activator AICAR (5-aminoimidazole-4-carboxamide1-β-D-ribofuranoside), or the AMPK inhibitor compound C, respectively. Cell proliferation was measured by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Intracellular lipid accumulation was observed after Oil Red O staining and determined by triglycerides (TG) and total cholesterol (TC) assay kits. The secretion of nitric oxide (NO) by HAECs was detected by nitrate reductase assay. The phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and endothelial nitric oxide synthase (eNOS) was measured by Western Blotting assay. Results: OA exposure inhibited cell proliferation and resulted in lipid accumulation in HAECs in a concentration-dependent manner. Co-treatment with berberine resulted in no significant differences in all tested parameters compared with the normal control group and showed significantly improved cell viability compared with treatment with OA alone (P < 0.01). The degree of lipid infiltration was higher after OA treatment compared with the normal control group. OA concentration-dependently induced lipid accumulation in endothelial cells, while lipid accumulation was significantly reduced by added berberine. OA significantly decreased NO levels compared with the normal control group, but this decrease was significantly reversed by berberine; furthermore, berberine repressed the increase caused by OA in reactive oxygen species (ROS). OA inhibited AMPK activation and consequently significantly attenuated the levels of p-AMPK and p-eNOS (P < 0.01). Accordingly, berberine could reverse the reduced phosphorylation of AMPK and eNOS induced by OA, but this effect was antagonized by Compound C. Conclusion: Berberine can alleviate endothelial cell injury induced by oleic acid, which may be due to the activation of the AMPK-eNOS signaling pathway.

Key words: berberine, oleic acid, adenosine monophosphate-activated protein kinase, nitric oxide synthase, human aortic endothelial cells

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