Tanshinone IIA Alleviates Atherosclerosis Through Inhibition of NF-κB and PPARα/ABCA1 Signaling Pathways

Abstract

This study evaluated the role and underlying mechanisms of Tanshinone IIA (Tan IIA) in atherosclerosis. C57BL mice (control group) and ApoE mice (model group) were administered a conventional and high-fat diet for 20 weeks. The Tan IIA group was obtained by administering a high-fat diet plus 8 weeks of Tan IIA to other mice for 20 weeks, followed by oil red O staining and lipid examination. RAW264.7 cells were transfected with PPAR α siRNA+Tan IIA to measure their expression. The results showed little change in body weight between the three groups ( P < 0.05). Liver index was significantly increased in the model and Tan IIA groups ( P <0.05). Atherosclerotic plaques, plaque cross-sectional area, human oxidized low-density lipoprotein (ox-LDL), low-density lipoprotein cholesterol (LDL-C) and triglyceride (TG) levels, p-NF- κ B, p-IKK α , P-Ikk α / β , TNF- α and IL-1 β levels were significantly increased in the model group and decreased in the Tan IIA group ( P < 0.05). We also noted a decrease in PPAR α , PGC-1 α and ABCA1 in the model group and an increase in the Tan IIA group. NF- κ B expression was increased in the nucleus and decreased in the cytoplasm in the model group, which was reversed by Tan IIA treatment. Tan IIA significantly reduced ox-LDL, LDL-C and TG levels, plaque size and plaque cross-sectional area in atherosclerosis. Tan IIA effectively inhibited NF- κ B, activated the PPAR α /ABCA1 signalling pathway, and reduce inflammatory pathways, thereby improving lipid deposition and acting as an anti-atherosclerotic agent.