|
Effect | Subjects | Possible mechanism | Reference |
|
Animals | | | |
Endothelial protection | Wistar rats | Neutralize ROS, protect mitochondrial membrane, reduce LPO, and increase GSH levels through the increased catalase activity | [109] |
ApoE−/− mice | Regulate NADPH oxidase subunits expression | [16] |
Sprague-Dawley rats | Increase GSH, erythrocyte CAT, and MDA levels | [50] |
Wistar rats | Decrease serum LDL, TC, MDA, and ROS to improve the vascular structure and prevent from the plaque formation | [101] |
|
Anti-inflammation | ApoE−/− mice | Decrease serum TNF-α and IL-6 levels and increase levels | [110] |
ApoE−/− mice | Inhibit phenotypic and functional maturation of DCs | [111] |
Balb/c mice | Mediate HDL function and lipid-glucose state in the circulation by improving biological activity (quality) and the activity of bound to PON1 | [112] |
|
Antiapoptosis | Nude mice | Activate ERK and the ERK signaling pathway to promote autophagy | [113] |
ApoE−/− mice | Enhance autophagy and downregulate mTOR, P53 and P21 protein expression levels to alleviate AS lesions and reduce lipid accumulation and increase ratio of LC3 II/I | [83] |
|
Regulate lipid metabolism and reduce the atherosclerotic plaque area | ApoE−/− mice | Increase ABCA1 and LXRα expression and downregulate PCSK9 protein expression | [110] |
Wistar rats | Elevate activity of hepatic CYP7A1, LXRα, and ABCG1 to promote cholesterol-to-bile acid conversion and cholesterol efflux | [114] |
C57BL/6J mice | Upregulate LDLR and CYP7A1 gene expression to facilitate the removal of cholesterol via fecal excretion | [115] |
Wistar rats | Promote conversion of cholesterol to bile acids and cholesterol efflux by increasing hepatic CYP7A1 activity and hepatic LXRα, ABCG1, and LDLR protein expressions | [116] |
ApoE−/− mice | Elevate cholesterol accepting ability of HDL and increase ABCA1/G1 expression levels of proteins related to RCT | [117] |
Sprague-Dawley rats | Influence gene and protein expression of SREBP1c and HMGR to lower lipid | [118] |
Sprague-Dawley rats | Upregulate hepatic gene expression CYP7A1, LXRα, ABCA1, and ABCG1 to promote cholesterol efflux | [119] |
Zucker rats | Lower the level of HDL cholesterol and increase phosphorus level by increasing the ratio of ASAT/ALAT activity induced by leptin | [56] |
ApoE−/− mice | Regulate expressions of ABCA1, LXRα, and PCSK9 | [26] |
ApoE−/− mice | Downregulate PCSK9 and CD36 protein expression and upregulate PPAR γ, LXRα, and ABCA1 protein expression levels in both the aortic and liver tissues | [65] |
|
Alter the gut microbiota | ApoE−/− mice | Regulate primary bile acid biosynthesis | [95] |
C57BL/6J mice | Improve composition and functionality of gut microbiome and production of short chain fatty acids | [120] |
Wistar rats | Stimulate bacterial enzymatic activity and increase enzymatic activity of the intestinal microbiota | [121] |
Ldlr−/− mice | Reduce MDA, cholesterol, and LPC 18 : 1 and increase IL-6 and coprostanol levels | [98] |
|
Humans | | | |
Anti-inflammation | Healthy nonsmokers | Inhibit production of IL-1β, TNF-α, IL-6, and IL-8 in Lipopolysaccharide-stimulated | [122] |
CVD patients | Decrease transcriptional activity of NF-kB | [74] |
Endothelial protection | CVD individuals | Enhance NO bioavailability, possibly by stimulating eNOS activity | [123] |
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