• Journal of Life Science
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• v.25 no.11
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• pp.1265-1272
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• 2015

Barnyard millet Miryang 3 [Echinochloa esculenta (A. Braun)] grains have recently been acknowledged for beneficial health properties due to phenolic ingredients and dietary fiber. This study has been conducted on the anti-diabetic activity of barnyard millet Miryang 3 which shows the strongest anti-inflammatory activity among barnyard millet inhabiting in South Korea. When 80% ethanol (EtOH) extract of barnyard millet Miryang 3 grains were orally administered into db/db diabetic mice for 8 weeks (600 mg/kg/day), the glucose level in blood following fasting appeared to be improved compared to the control group. The results of glucose tolerance test and blood lipid profile assay were similar to those of the metformin-administered positive control group. In addition, the level of body weight increase (8.54±2.24) was lower than the level of metformin-administered group (10.36±3.15); however, there was no subtle difference with negative and positive control groups in terms of food efficiency rates. In addition, total cholesterol levels of the 80% EtOH extract-administered group (160.7±7.6) were significantly reduced compared to the diabetic control group (229.3±47.8) and metformin-administered group (176.0±25.6). Consequently, these results show that barnyard millet grains alleviates many of the diabetic symptoms in vivo non-insulin-dependent diabetes mellitus, and suggest that barnyard millet grains can be applicable in developing new functional food materials.

• Journal of Microbiology and Biotechnology
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• v.27 no.1
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• pp.197-205
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• 2017

Exposure of Jurkat T cell clone (J/Neo cells) to acacetin (5,7-dihydroxy-4'-methoxyflavone), which is present in barnyard millet (Echinochloa esculenta (A. Braun)) grains, caused cytotoxicity, enhancement of apoptotic $sub-G_1$ rate, Bak activation, loss of mitochondrial membrane potential (${\Delta}{\Psi}m$), activation of caspase-9 and caspase-3, degradation of poly(ADP-ribose) polymerase, and FITC-Annexin V-stainable phosphatidylserine exposure on the external surface of the cytoplasmic membrane without accompanying necrosis. These apoptotic responses were abrogated in Jurkat T cell clone (J/Bcl-xL) overexpressing Bcl-xL. Under the same conditions, cellular autophagic responses, including suppression of the Akt-mTOR pathway and p62/SQSTM1 down-regulation, were commonly detected in J/Neo and J/Bcl-xL cells; however, formation of acridine orange-stainable acidic vascular organelles, LC3-I/II conversion, and Beclin-1 phosphorylation (Ser-15) were detected only in J/Neo cells. Correspondingly, concomitant treatment with the autophagy inhibitor (3-methyladenine or LY294002) appeared to enhance acacetin-induced apoptotic responses, such as Bak activation, ${\Delta}{\Psi}m$ loss, activation of caspase-9 and caspase-3, and apoptotic $sub-G_1$ accumulation. This indicated that acacetin could induce apoptosis and cytoprotective autophagy in Jurkat T cells simultaneously. Together, these results demonstrate that acacetin induces not only apoptotic cell death via activation of Bak, loss of ${\Delta}{\Psi}m$, and activation of the mitochondrial caspase cascade, but also cytoprotective autophagy resulting from suppression of the Akt-mTOR pathway. Furthermore, pharmacologic inhibition of the autophagy pathway augments the activation of Bak and resultant mitochondrial damage-mediated apoptosis in Jurkat T cells.