Abstract
Atherosclerosis is a major reason for the high morbidity and mortality of cardiovascular diseases. Macrophage inflammation and foam cell formation are the key pathological processes of atherosclerosis. Ginsenoside compound K (CK) is a metabolite derived from ginseng. CK has anti atherosclerotic effect, but the molecular mechanism remains to be elucidated. We aim to explore the protective effect of CK against ox-LDL-induced inflammatory responses and foam cells formation in vitro and explore its potential mechanisms. Through the results of oil red O staining, Western blot, and qPCR, we found that CK significantly inhibited the foam cell formation, reduced the expression of SR-A1 and increased ABCA1 and ABCG1 expression. In addition, CK increased the number of autophagosomes and upregulated the LC3II/LC3I ratio and the expressions of ATG5 and Beclin-1 but decreased p62 expression. Moreover, CK significantly inhibited the NF-κB, p38, and JNK MAPK signaling pathway. Altogether, CK attenuated macrophage inflammation and foam cell formation via autophagy induction and by modulating NF-κB, p38, and JNK MAPK signaling. Thus, CK has potential as a therapeutic drug for atherosclerosis.
Highlights
Atherosclerosis is the leading cause of coronary heart disease and poses threat to the health of humans worldwide (Virani et al, 2020)
Ox-LDL-induced macrophage-derived foam cell is an important factor in the formation of early atherosclerotic plaques (Glass and Witztum, 2001)
According to oil red O results (Figures 1C, D), lipid accumulation was increased by oxidized low-density lipoprotein (ox-LDL), whereas it was decreased in the group treated with compound K (CK) at different concentrations
Summary
Atherosclerosis is the leading cause of coronary heart disease and poses threat to the health of humans worldwide (Virani et al, 2020). It is a complex disease characterized by lipid accumulation within the arterial wall, and vascular cells are involved. In the early stages of atherosclerosis, macrophages take up a large amount of oxidized low-density lipoprotein (ox-LDL) to produce foam cells. The formation of macrophage foam cells further aggravates atherosclerotic lesions. Theox-LDL stimulates macrophages to produce multiple inflammatory factors, further affecting macrophage cholesterol efflux and aggravating plaque formation (Libby et al, 2002). Foam cell formation and macrophage inflammation are potential strategies in atherosclerosis treatment
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