Inflammation is a major contributing factor to the progression of
atherosclerosis.
Ginsenoside Rb1 (Rb1), an active
saponin of Panax notoginseng, has been found to exert beneficial effects on
inflammation and oxidative stress. This study investigated the ability of Rb1 to inhibit the formation of
atherosclerotic plaques and the potential mechanisms. In this study, the effects of Rb1 on the development of
atherosclerosis were investigated in
ApoE-/- deficient mice fed with a western diet. Mice were intragastrically administrated with Rb1 (10 mg/kg) for 8 weeks. This study is that
ginsenoside Rb1 exerted an inhibitory effect on early
atherosclerosis in
ApoE-/- mice via decreasing
body weight and food intake daily, upregulating the
lipid levels of serum plasma, including those of TC, TG and
LDL-C and HDL-C and reducing the
atherosclerotic plaque area, suppressing inflammatory
cytokines (levels of IL-1β, IL-6 and TNF-α) in the serum of
ApoE-/- mice, changing the expression levels of BCL-2, BAX, cleaved
caspase-3 and cleaved
caspase-9 and weakening apoptosis associated with anti-inflammatory activity. Hence, all these effects against
atherosclerosis were tightly associated with regulation of
necrosis or apoptosis associated with anti-inflammatory activity. Additionally, the results found that
ginsenoside Rb1 increased autophagy flux to inhibit apoptosis via acceleration of autophagy by promoting transformation of LC3 from type I to type II in high-fat diet-induced
atherosclerosis in
ApoE-/- mice. This finding, along with those of the previous study, provides evidence that Rb1 promotes the process of autophagy to protect against
atherosclerosis via regulating BCL-2 family-related apoptosis. These results indicate that Rb1 exhibits
therapeutic effects in
atherosclerosis by reversing the imbalance between apoptosis and autophagy.