Shexiang Baoxin Pill Alleviates the Atherosclerotic Lesions in Mice via Improving Inflammation Response and Inhibiting Lipid Accumulation in the Arterial Wall

Figure 7

Schematic description of the protective mechanisms by which SBP attenuated the development of atherosclerosis in apoE^-/- mice fed by HFD. ROS and proinflammatory cytokines activated the signaling molecules including NF-κB, JNK, and p38 to promote the production of inflammation factors. SBP treatment increased the level of Mfn2 and then suppressed the activities of NF-κB, JNK, and p38, thereby reducing the generation of inflammatory cytokines and monocyte accumulation. Meanwhile, SBP elevated the contents of reverse cholesterol transporters and reduced the levels of scavenger receptors via regulating the signal transduction of relevant pathways in the vascular wall, which reduced the lipid influx and accelerated the efflux, leading to repression of foam cell formation.