Study On The Mechanism Of Anti-atherosclerosis By Phlegm And Blood Stasis

ObjectivesAtherosclerosis is a relatively common kind of cardiovascular disease, which is the pathological physiological basis and the main cause of a variety of disease, such as coronary heart disease (CHD) and stroke. It has been the key threat to human health and living quality. We study the biological basis of syndrome of intermin-gled phlegm and blood stasis in atherosclerosis by animal model and cell model, and investigate the mechanism of the syndrome after treating the animals or cells with Qutan Huayu prescription(QTHYF) in order to provide reference for clinical treatment.Materials and Methods1. ApoE-/- mice were used to form the animal model of hyperlipidemia and atherosclerosis by being fed with western diet.2. We detected the lipid level, the ratio of circulating monocytes with its TLR4 and the cytokine levels in plasma(after 3h-stimulated by LPS) as well as aorta of ApoE-/- mice treated with QTHYF, to evaluate the effect of QTHYF.3. The cell model was built, which represents different developmental stages of atherosclerosis:monocyte, macrophage, and foam cell.4. The phenotype and function of cells mentioned above were detected by flow cytometry and real-time PCR after treating with serum containing QTHYF in order to evaluate its impact on monocyte, macrophage, and foam cell.Results1. QTHYF increases the ratio of Ly6C- monocytes while decreasing Ly6C++ monocytes in the peripheral blood of ApoE-/- mice.2. QTHYF reduces inflammatory cytokine levels in the peripheral blood(after 3h-stimulated by LPS) of ApoE-/- mice, such as TNF-α, IFN-γ, IL-12, IL-6 and MCP-1.3. QTHYF inhibits mRNA levels of inflammatory cytokines in the aorta like IL-6, IL-1β, MCP-1 and TNF-a, while promoting mRNA express of anti-inflammatory cytokines such as TGF-β,IL-10 and Arg-1.4. Serum containing QTHYF accelerates monocyte to differentiate into M2 macrophage, along with the increase of CD206 and Argl as well as the decrease of NOS2. 5. Serum containing QTHYF promotes macrophage polarizing to M2 macrophage, accompaning with the increase of CD206 and Arg1 as well as the decrease of NOS2.ConclusionsIn vivo, QTHYF can transform the ratio of different subsets of monocytes and cytokines with different functions to inhibit the systemic inflammatory response, while reducing the inflammatory cytokines in the aorta to suppress vascular inflammatory response. In vitro, serum containing QTHYF can inhibit atherosclerosis by regulating differentiation of monocytes and macrophages.