Abstract
ObjectiveThe aim of this study was to explore potential immunoregulatory mechanisms underlying the suppressive effect on atherosclerosis of QiShenYiQi pill (QSYQ).Methods and ResultsMale ApoE-/- mice were maintained on a Western-type diet and QSYQ treatment for eight weeks. Determination of atherosclerosis demonstrated that QSYQ attenuated plaque formation and decreased the level of blood low-density lipoproteins-cholesterol. QSYQ treatment did not affect body weight but reduced the ratio of liver weight and body weight. Western blots of liver showed that QSYQ increased the expression of liver X receptor alpha and ATP-binding cassette sub-family G member 5. Western blots of atherosclerotic aorta revealed that QSYQ inhibited the expression of cluster of differentiation 36, promoted the expression of forkhead box P3 and decreased interleukin-17A expression. Western blots of spleen showed that QSYQ decreased the expression of mothers against decapentaplegic homolog 2/3 and forkhead box P3, as well as attenuated the expression of spleen interleukin-6, RAR-related orphan receptor gamma and interleukin-17A.ConclusionsQSYQ exerted an anti-atherosclerosis effect by promoting regulatory T cells in atherosclerotic lesion, inhibiting T helper 17 cells in plaque and spleen and accelerating liver cholesterol excretion.
Highlights
Atherosclerosis is a chronic inflammatory disease [1]
Determination of atherosclerosis demonstrated that QSYQ attenuated plaque formation and decreased the level of blood low-density lipoproteins-cholesterol
Western blots of liver showed that QSYQ increased the expression of liver X receptor alpha and ATP-binding cassette sub-family G member 5
Summary
Atherosclerosis is a chronic inflammatory disease [1]. Immune responses participate in every phase of atherosclerosis [2]. Published evidence shows that both innate and adaptive immune responses are involved in atherogenesis, but the precise molecular mechanisms of these responses are not well understood [3]. When lowdensity lipoproteins (LDL) accumulate in the intima, endothelial cells become activated and express cell adhesion molecules, chemokines and other mediators, which promote circulating monocyte rolling on and adhering to the endothelium. Monocytes infiltrate the subendothelial space to initiate the formation of atherosclerotic plaques. Mononuclear macrophages can take up oxidized-LDL through scavenger receptors, such as cluster of differentiation 36 (CD36) [4, 5], and/ or release toll-like receptor-mediated pro-inflammatory cytokines, chemokines, and proteases during innate immune responses [6]
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