Effects of blackcurrant-based juice on atherosclerosis-related biomarkers in cultured macrophages and in human subjects after consumption of a high-energy meal.
Regular consumption of fruit and vegetables may be associated with decreased CVD risk. In the present study, we investigated the effects of blackcurrant (BC) juice, rich in polyphenols and ascorbic acid, on oxidative and inflammatory biomarkers in cultured macrophages in vitro and in human subjects with an atherosclerosis-prone phenotype (after consumption of a high-energy meal). In cultured macrophages (RAW264.7), BC treatment significantly inhibited lipopolysaccharide-induced inflammation as indicated by lower mRNA levels of TNF-α, IL-1β and inducible NO synthase (iNOS) and lower nuclear p65 levels indicating decreased NF-κB activity. iNOS protein levels were lower and haem oxygenase 1 levels higher in BC-treated cells when compared with untreated controls. Subjects given a high-energy meal had elevated serum glucose and insulin levels with no significant difference between the BC-based juice and placebo treatment groups. TAG following meal ingestion tended to be attenuated after the BC treatment. Plasma ascorbic acid and radical-scavenging capacity were decreased following placebo meal consumption; however, BC significantly elevated both parameters compared with baseline and placebo ingestion. Plasma oxidised LDL, α-tocopherol and paraoxonase activity were unchanged in both treatment groups. Furthermore, production of TNF-α and IL-1β was not significantly changed by BC meal consumption. The present results suggest potential antioxidative and anti-inflammatory properties of BC in vitro in cultured macrophages. Although the observations were not directly transferable to a postprandial in vivo situation, the present results show that BC juice consumption may improve postprandial antioxidant status as indicated by higher ascorbic acid levels and free radical-scavenging capacity in plasma.
Institute of Human Nutrition and Food Science, Christian-Albrechts-University of Kiel, Kiel, Germany.
Patricia
P
Huebbe
Katrin
K
Giller
Sonia
S
de Pascual-Teresa
Anne
A
Arkenau
Berit
B
Adolphi
Sebastian
S
Portius
Cord N
CN
Arkenau
Gerald
G
Rimbach
D000328:Adult; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000378:metabolism / Q000627:therapeutic use; D000975:Antioxidants / Q000032:analysis / Q000378:metabolism; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000097:blood* / Q000378:metabolism; D050197:Atherosclerosis / Q000097:blood* / Q000276:immunology / Q000517:prevention & control; D001628:Beverages; D002461:Cell Line, Transformed; D018592:Cross-Over Studies; D004036:Diet, Atherogenic / Q000009:adverse effects; D015536:Down-Regulation; D005638:Fruit / Q000737:chemistry*; D006801:Humans; D015228:Hypertriglyceridemia / Q000517:prevention & control; D018836:Inflammation Mediators / Q000097:blood / Q000378:metabolism*; D008264:Macrophages / Q000201:enzymology / Q000276:immunology / Q000378:metabolism*; D008297:Male; D051379:Mice; D052247:Nitric Oxide Synthase Type II / Q000235:genetics / Q000378:metabolism; D018384:Oxidative Stress; D019518:Postprandial Period; D031965:Ribes / Q000737:chemistry*; D016037:Single-Blind Method
D000894:Anti-Inflammatory Agents, Non-Steroidal; D000975:Antioxidants; D018836:Inflammation Mediators; D052247:Nitric Oxide Synthase Type II; C496317:Nos2 protein, mouse; D001205:Ascorbic Acid