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  • Title: Puerarin protects vascular smooth muscle cells from oxidized low-density lipoprotein-induced reductions in viability via inhibition of the p38 MAPK and JNK signaling pathways.
    Author: Hu Y, Li H, Li R, Wu Z, Yang W, Qu W.
    Journal: Exp Ther Med; 2020 Dec; 20(6):270. PubMed ID: 33199995.
    Abstract:
    Puerarin belongs to the family of flavonoids extracted from Pueraria lobata (Wild.) Ohwi, which exhibits antioxidative, anti-inflammatory, anti-hyperglycemic, antitumor, anti-hypertensive and anti-atherosclerotic activities. In the present study, the effects of puerarin on oxidized low-density lipoprotein (ox-LDL)-stimulated vascular smooth muscle cells (VSMCs) were explored to understand the mechanisms underlying the anti-atherosclerotic effects of puerarin. VSMCs were treated with various concentrations of puerarin (0, 20, 40 and 80 µM) prior to stimulation with ox-LDL (50 µg/ml). VSMC viability was evaluated by performing MTT and Cell Counting Kit-8 assays. Moreover, superoxide dismutase (SOD) and malondialdehyde (MDA) levels were measured by performing ELISAs. The mRNA expression levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were determined via reverse transcription-quantitative PCR. Western blotting was conducted to assess the levels of p38-MAPK and JNK phosphorylation. The results indicated that puerarin inhibited ox-LDL-induced VSMC viability. Moreover, puerarin significantly decreased the mRNA expression levels of IL-6 and TNF-α, significantly reduced the production of MDA and significantly increased SOD activity in ox-LDL-stimulated VSMCs. Puerarin also inhibited ox-LDL-induced phosphorylation of p38 and JNK in VSMCs. The results suggested that puerarin reduced ox-LDL-induced VSMC viability via inhibition of the p38 MAPK and JNK signaling pathways. The present study provided theoretical evidence that puerarin may serve as a therapeutic agent to reduce the development of atherosclerosis.
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