Inhibitory Effect of Black Radish (Raphanus sativus L. var. niger) Extracts on Lipopolysaccharide-Induced Inflammatory Response in the Mouse Monocyte/Macrophage-Like Cell Line RAW 264.7.

Black radish (Raphanus sativus L. var. niger), which is cultivated worldwide, is used in traditional medicine as it aids liver function, gastric secretion, gallbladder function, and gallstone mitigation. In this study, we examined the anti-inflammatory effects of black radish extract (BRE) on the lipopolysaccharide (LPS)- and interleukin (IL)-6-mediated inflammatory responses in the RAW 264.7 cell lines. Our findings show that BRE significantly ameliorated LPS-induced nitric oxide (NO) release and production of pro-inflammatory cytokines, such as IL-1ß, IL-6, tumor necrosis factor (TNF)-α, and prostaglandin E2. The levels of cyclooxygenase (COX)-2 and inducible NO synthase (iNOS) in LPS-stimulated RAW 264.7 cells were found to be suppressed by BRE. Further, BRE significantly suppressed the LPS-induced expression of mRNAs encoding COX-2, iNOS, IL-1ß, IL-6, and TNF-α in a concentration-dependent manner. BRE treatment significantly inhibited Janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) phosphorylation in IL-6- and LPS-treated RAW 264.7 cells. In addition, BRE decreased the levels of phosphorylated extracellular signal-regulated protein kinases and c-Jun N-terminal kinase under the same conditions. Moreover, BRE induced high nuclear factor erythroid 2-related factor 2 (NRF2) levels and its target gene heme oxygenase 1 (HO-1) in the absence of LPS. These data demonstrate that BRE may be beneficial for treating inflammation through selective immunomodulatory effects, which may be mediated by inhibition of the STAT3/JAK2 and activation of the NRF2/HO-1 signal transduction pathways.

Fermented black radish (Raphanus sativus L. var. niger) attenuates methionine and choline deficient diet-induced nonalcoholic fatty liver disease in mice.

As one of the wide-ranging form of chronic liver disease, there are only limited therapeutic options for nonalcoholic fatty liver disease (NAFLD). We evaluated whether fermented black radish (Raphanus sativus L. var. niger; FBR) ameliorates lipid accumulation, inflammation, and hepatic fibrosis, which are characteristics of the pathogenesis of NAFLD. Fermented black radish treatment reduced lipid accumulation in 3T3-L1 adipocytes, which appeared to be associated with the downregulation of adipogenic transcription factors, including sterol regulatory element-binding protein 1c, CCAAT/enhancer-binding protein α, peroxisome proliferator-activated receptor γ, and lipid accumulation-related genes including adipocyte protein-2 and fatty acid synthase. Administration of FBR to C57BL/6J mice challenged with methionine and choline deficient (MCD) diet significantly attenuated the increased serum levels of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and triglyceride. In addition, treatment with FBR interestingly repressed the hepatic inflammation induced with MCD diet, by lowering the expression of inducible nitric oxide synthase and suppressing the inactivation of macrophages and Kupffer cells in the liver. Fermented black radish was also shown to mitigate liver fibrosis through the inhibition of alpha-smooth muscle actin, transforming growth factor beta-1, and collagen type I alpha 1 chain. Our results indicate that FBR ameliorates NAFLD and its related metabolic disease by regulating multiple pathways, suggesting that FBR may be an effective dietary supplement for ameliorating NAFLD.

Protective effect of ixerisoside A against UVB-induced pro-inflammatory cytokine production in human keratinocytes.

Human skin is the first line of defense for the protection of the internal organs of the body from different stimuli. Ultraviolet B (UVB), one of the harmful radiations for skin, is widely known to induce abnormally increased cytokine release from keratinocytes leading to inflammatory skin disorders. IL-6 and IL-8 induce an acute-phase response and stimulate leukocyte infiltration in the skin. Previous studies have shown that chronic exposure to UVB radiation increases cyclooxygenase-2 (COX­2) expression through various cell signaling pathways, resulting in skin cancer. Recent studies have shown that the activation of extracellular signal-regulated kinase (ERK), c-Jun NH2-terminal kinase (JNK), and p38 MAPK is strongly correlated with acute inflammation and development of skin cancer caused by an increased expression of COX-2. Ixerisoside A (IXA) is an active constituent of Ixeris dentata of the Compositae (Asteraceae) family. The effect of IXA on skin inflammation has yet to be elucidated. To determine the anti-inflammatory effects of IXA, we examined its effect on UVB-induced pro-inflammatory cytokine production in human keratinocytes (HaCaT cells) by observing these cells in the presence or absence of IXA. In this study, pro-inflammatory cytokine production was determined by enzyme-linked immunosorbent assay (ELISA), reverse transcription-polymerase chain reaction (rt-pcr), and western blot analysis to evaluate the activation of mitogen-activated protein kinases (MAPKs). IXA inhibited UVB-induced production of the pro-inflammatory cytokines IL-6 and IL-8 in a dose-dependent manner. Moreover, IXA inhibited the expression of COX-2, ERK, JNK, and p38 MAPKs, indicating that the secretion of the pro-inflammatory cytokines IL-6 and IL-8, and COX-2 expression was inhibited by blocking MAPK phosphorylation. These results indicated that IXA potentially protects against UVB-induced skin inflammation.