Ginsenoside compound K protects human umbilical vein endothelial cells against oxidized low-density lipoprotein-induced injury via inhibition of nuclear factor-kB, p38, and JNK MAPK pathways

Shan Lu; Yun Luo; Ping Zhou; Ke Yang; Guibo Sun; Xiaobo Sun

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자료유형: 학술저널

저자정보: Shan Lu (Peking Union Medical College and Chinese Academy of Medical Sciences) Yun Luo (Peking Union Medical College and Chinese Academy of Medical Sciences) Ping Zhou (Peking Union Medical College and Chinese Academy of Medical Sciences) Ke Yang (Peking Union Medical College and Chinese Academy of Medical Sciences) Guibo Sun (Peking Union Medical College and Chinese Academy of Medical Sciences) Xiaobo Sun (Peking Union Medical College and Chinese Academy of Medical Sciences)

저널정보: 고려인삼학회 Journal of Ginseng Research Journal of Ginseng Research Vol.43 No.1

발행연도: 2019.1

수록면: 95 - 104 (10page)

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Background: Oxidized low-density lipoprotein (ox-LDL) causes vascular endothelial cell inflammatory response and apoptosis and plays an important role in the development and progression of atherosclerosis. Ginsenoside compound K (CK), a metabolite produced by the hydrolysis of ginsenoside Rb1, possesses strong anti-inflammatory effects. However, whether or not CK protects ox-LDL-damaged endothelial cells and the potential mechanisms have not been elucidated.
Methods: In our study, cell viability was tested using a 3-(4, 5-dimethylthiazol-2yl-)-2,5-diphenyl tetrazolium bromide (MTT) assay. Expression levels of interleukin-6, monocyte chemoattractant protein-1, tumor necrosis factor-α, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 were determined by enzyme-linked immunosorbent assay and Western blotting. Mitochondrial membrane potential (DJm) was detected using JC-1. The cell apoptotic percentage was measured by the Annexin V/ propidium iodide (PI) assay, lactate dehydrogenase, and caspase-3 expression. Apoptosis-related proteins, nuclear factor (NF)-kB, and mitogen-activated protein kinases (MAPK) signaling pathways protein expression were quantified by Western blotting.
Results: Our results demonstrated that CK could ameliorate ox-LDL-induced human umbilical vein endothelial cells (HUVECs) inflammation and apoptosis, NF-kB nuclear translocation, and the phosphorylation of p38 and c-Jun N-terminal kinase (JNK). Moreover, anisomycin, an activator of p38 and JNK, significantly abolished the anti-apoptotic effects of CK.
Conclusion: These results demonstrate that CK prevents ox-LDL-induced HUVECs inflammation and apoptosis through inhibiting the NF-kB, p38, and JNK MAPK signaling pathways. Thus, CK is a candidate drug for atherosclerosis treatment.

#apoptosis #ginsenoside compound K #human umbilical vein endothelial cells #inflammation #oxidized low-density lipoprotein

참고문헌 (33)

참고문헌 신청

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