Influence of extraction method on quality and functionality of broccoli juice.

This study was performed to compare the quality and functionality of broccoli juice as affected by extraction method. Broccoli juice was extracted using method I (NUC Kuvings silent juicer), method II (NUC centrifugal juicer), and method III (NUC mixer), and the quality properties of the broccoli juices were analyzed using three different methods. Additionally, the antioxidative, anticancer, and anti-hyperglycemic activities of broccoli juice prepared by the three different methods were investigated in vitro. The broccoli juice made by method I contained the highest polyphenol and flavonoid contents at 1,226.24 mg/L and 1,018.32 mg/L, respectively. Particularly, broccoli juice prepared by method I showed higher DPPH and ABTS radical scavenging activities than those of the other samples. Additionally, broccoli juice made by method I showed the highest growth inhibitory effects against HeLa, A549, AGS, and HT-29 cancer cells. Broccoli juice prepared by method I had the highest α-glucosidase inhibitory effects. These results indicate that there are important differences in chemical and functional qualities between juice extraction techniques.

Anti-inflammatory and anti-osteoarthritis effects of fermented Achyranthes japonica Nakai.

ETHNOPHARMACOLOGICAL RELEVANCE: Achyranthyes japonica Nakai (AJN) has been traditionally used to control pain and improve dysfunction in osteoarthritis (OA) patients. AIM OF THE STUDY: The objectives of the present study were to investigate anti-inflammatory and anti-osteoarthritis activities of fermented AJN (FAJN). MATERIALS AND METHODS: Anti-inflammatory activity of non-fermented AJN (NFAJN) and FAJN was evaluated by in vitro assay using LPS-induced RAW 264.7 cells. In addition, their cartilage protective effects were also determined in vitro assay using SW1353 cell and in vivo model system using collagenase-induced arthritis (CIA) in rabbits. Moreover, we isolated and identified 20-hydroxyecdysone (20-HES) as a marker component in FAJN. RESULT: FAJN showed stronger anti-inflammatory activity than NFAJN through inhibiting production of NO and PGE2 in LPS-induced RAW 264.7, and lowering levels of MMP-3 release in SW1353 cells treated with TNF-a. FAJN contained higher levels of 20-HES, as a marker component, than AJN. FAJN ameliorates the progress of OA by inhibiting local inflammation. It does this by regulating levels of TNF-a and IL-4, and protecting articular cartilage by preventing destruction of proteoglycan, collagens, and also preventing injury to chondrocytes. CONCLUSION: Therefore, FAJN is a potential therapeutic agent for reduction of cartilage damage that occurs in OA.

Tectoridin, a poor ligand of estrogen receptor alpha, exerts its estrogenic effects via an ERK-dependent pathway.

Phytoestrogens are the natural compounds isolated from plants, which are structurally similar to animal estrogen, 17beta-estradiol. Tectoridin, a major isoflavone isolated from the rhizome of Belamcanda chinensis. Tectoridin is known as a phytoestrogen, however, the molecular mechanisms underlying its estrogenic effect are remained unclear. In this study we investigated the estrogenic signaling triggered by tectoridin as compared to a famous phytoestrogen, genistein in MCF-7 human breast cancer cells. Tectoridin scarcely binds to ER alpha as compared to 17beta-estradiol and genistein. Despite poor binding to ER alpha, tectoridin induced potent estrogenic effects, namely recovery of the population of cells in the S-phase after serum starvation, transactivation of the estrogen response element, and induction of MCF-7 cell proliferation. The tectoridin-induced estrogenic effect was severely abrogated by treatment with U0126, a specific MEK1/2 inhibitor. Tectoridin promoted phosphorylation of ERK1/2, but did not affect phosphorylation of ER alpha at Ser(118). It also increased cellular accumulation of cAMP, a hallmark of GPR30-mediated estrogen signaling. These data imply that tectoridin exerts its estrogenic effect mainly via the GPR30 and ERK-mediated rapid nongenomic estrogen signaling pathway. This property of tectoridin sets it aside from genistein where it exerts the estrogenic effects via both an ER-dependent genomic pathway and a GPR30-dependent nongenomic pathway.