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

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.