Blackcurrant (Ribes nigrum) and Inflammation (general): evidence and sources

The blackcurrant (Ribes nigrum L., Grossulariceae), a small, perennial shrub native to central Europe and northern Asia, is cultivated throughout the world, including the United States. In addition to its anecdotal use in traditional herbal medicine, modern laboratories have demonstrated the potent anti-inflammatory, antioxidant and antimicrobial effects of blackcurrant constituents on a myriad of disease states. The properties of the blackcurrants are conferred from its biochemical constituents, some of which include anthocyans (specifically delphinidin-3-O-glucoside, delphinidin-3-O-rutinoside, cyanidin-3-O-glucoside and cyanidin-3-O-rutinoside), flavonols, phenolic acids and polyunsaturated fatty acids. A plethora of studies have been published with regards to its various therapeutic applications. This article attempts to summarize these studies, providing a general overview of the research in this field. Several studies focus on the therapeutic potential of blackcurrants with regards to hypertension and other cardiovascular-associated illnesses, neoplastic, neurodegenerative and ocular diseases, nephrolithiasis, and diabetic neuropathy. Safety concerns and future directions are also mentioned, suggesting the critical examination of the exact mechanism of action, specific radical-scavenging capabilities of the blackcurrants and the crucial need for well-designed clinical trials to ensure the successful use of blackcurrants in a clinical setting.

Objective With increasing prevalence of nonalcoholic steatohepatitis (NASH), effective strategies to prevent NASH are needed. This study investigated whether the consumption of blackcurrant (Ribes nigrum) can prevent the development of obesity-induced NASH in vivo. Methods Male C57BL/6J mice were fed a low-fat control diet, a low-fat diet with 6% whole blackcurrant powder, an obesogenic high-fat/high-sucrose control diet (HF), or a high-fat/high-sucrose diet containing 6% whole blackcurrant powder (HF-B) for 24 weeks. Results HF significantly increased, whereas HF-B markedly decreased, liver weights and triglyceride. Furthermore, blackcurrant attenuated obesity-induced infiltration of macrophages in the liver, in particular, the M1 type, and also suppressed the hepatic expression of fibrogenic genes and fibrosis. Flow cytometric analysis showed that HF significantly increased the percentages of monocytes of total splenocytes, which was markedly attenuated by blackcurrant. HF-B decreased lipopolysaccharide-stimulated mRNA expression of interleukin 1β and tumor necrosis factor α in splenocytes, compared with those from HF controls. Moreover, the levels of circulating and hepatic miR-122-5p and miR-192-5p, known markers for nonalcoholic fatty liver disease, were significantly increased by HF but decreased by HF-B. Conclusions The study's findings indicate that blackcurrant consumption prevents obesity-induced steatosis, inflammation, and fibrosis in the liver.

Macrophages are polarized into different phenotypes depending on tissue microenvironment where they reside. In obesity-associated inflammation, M1-type macrophages are predominant in the inflamed tissue, exerting pro-inflammatory responses. Our previous studies demonstrate that blackcurrant consumption attenuates hepatic inflammation and lipopolysaccharide-stimulated inflammatory responses of splenocytes in obese mice. In this study, we determined whether blackcurrant modulates macrophage phenotypes to exert its anti-inflammatory action. Mouse bone marrow-derived macrophages (BMDM) and human THP-1 macrophages were polarized into M1 macrophages in the presence or absence of blackcurrant extract (BCE). BCE repressed M1 polarization of both murine and human macrophages. Also, to gain insight into the role of blackcurrant metabolites produced in vivo in the regulation of macrophage phenotypes, BMDM were treated with serum obtained from lean or obese mice fed blackcurrant. While serum from lean mice fed blackcurrant did not exert either anti-inflammatory actions or suppressive effects on M1 polarization, serum from obese mice fed blackcurrant reduced the expression of pro-inflammatory genes in BMDM. Our data demonstrate that BCE suppresses M1 polarization, with reduced pro-inflammatory responses. Moreover, this study suggests that blackcurrant metabolites may not exert their anti-inflammatory effect directly by altering macrophage phenotypes, but possibly by inhibiting the production of obesity-associated inflammatory factors.