Nutritional and functional roles of millets-A review.

The available cultivable plant-based food resources in developing tropical countries are inadequate to supply proteins for both human and animals. Such limition of available plant food sources are due to shrinking of agricultural land, rapid urbanization, climate change, and tough competition between food and feed industries for existing food and feed crops. However, the cheapest food materials are those that are derived from plant sources which although they occur in abundance in nature, are still underutilized. At this juncture, identification, evaluation, and introduction of underexploited millet crops, including crops of tribal utility which are generally rich in protein is one of the long-term viable solutions for a sustainable supply of food and feed materials. In view of the above, the present review endeavors to highlight the nutritional and functional potential of underexploited millet crops. PRACTICAL APPLICATIONS: Millets are an important food crop at a global level with a significant economic impact on developing countries. Millets have advantageous characteristics as they are drought and pest-resistance grains. Millets are considered as high-energy yielding nourishing foods which help in addressing malnutrition. Millet-based foods are considered as potential prebiotic and probiotics with prospective health benefits. Grains of these millet species are widely consumed as a source of traditional medicines and important food to preserve health.

Neferine from Nelumbo nucifera modulates oxidative stress and cytokines production during hypoxia in human peripheral blood mononuclear cells.

Neferine, an alkaloid from N. nucifera has a broad range of pharmacological activity. Hypoxia mediated stress is involved in the generation of inflammatory responses and cell death. The present study evaluated the protective effect of neferine against hypoxia-induced cytotoxicity, oxidative stress and inflammatory response in human Peripheral Blood Mononuclear Cells (hPBMC). Cytotoxicity, as determined by MTT, LDH and NO assays revealed that 24h of hypoxic exposure results in 20% cell death (IC20) and compromising of cellular integrity, which was restored to near control values by pretreatment with neferine. Oxidative stress parameters such as lipid peroxidation and antioxidant enzymes indicated that neferine exerted a protective effect on hypoxia-induced oxidative stress. Hypoxia-induced Tumor Necrosis Factor-α (TNF-α), Interleukin 6 (IL-6), and Interleukin 8 (IL-8) release were significantly reduced in the neferine pretreated samples indicating its anti-inflammatory role. Our results demonstrate for the first time that neferine exerts a cytoprotective effect against hypoxia-induced oxidative stress and inflammation in hPBMC.

Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress.

BACKGROUND: Embryonic rhabdomyosarcoma (RD) is the most prevalent type of cancer among children. The present study aimed to investigate cell death induced by mangiferin in RD cells. METHODS: The Inhibitory concentration (IC50) value of mangiferin was determined by an MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay. Cell death induced by mangiferin against RD cells was determined through lactate dehydrogenase and nitric oxide release, intracellular calcium levels, reactive oxygen species generation, antioxidant status, mitochondrial calcium level, and mitochondrial membrane potential. Furthermore, acridine orange/ethidium bromide staining was performed to determine early/late apoptotic event. RESULTS: Mangiferin induced cell death in RD cells with an IC50 value of 70 µM. The cytotoxic effect was reflected in a dose-dependent increase in lactate dehydrogenase leakage and nitric oxide release during mangiferin treatment. Mangiferin caused dose dependent increase in reactive oxygen species generation, intracellular calcium levels with subsequent decrease in antioxidant status (catalase, superoxide dismutase, glutathione-S-transferase, and glutathione) and loss of mitochondrial membrane potential in RD cells. Further data from fluorescence microscopy suggest that mangiferin caused cell shrinkage and nuclear condensation along with the occurrence of a late event of apoptosis. CONCLUSION: Results of the present study shows that mangiferin can act as a promising chemopreventive agent against RD by inducing sustained oxidative stress.

Neferine, a bisbenzylisoquinoline alkaloid, offers protection against cobalt chloride-mediated hypoxia-induced oxidative stress in muscle cells.

BACKGROUND: Neferine, a bisbenzylisoquinoline alkaloid, isolated from Nelumbo nucifera has a wide range of biological activities. Cobalt chloride (CoCl2) was known to mimic hypoxic condition. In the present study, we assessed the cytoprotective effect of neferine against CoCl2-induced oxidative stress in muscle cells. METHODS: Rhabdomyosarcoma cells were exposed to different concentrations of CoCl2, and the IC50 value was determined using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Lactate dehydrogenase and NO assays were performed in order to determine the cytotoxic effect of CoCl2. Reactive oxygen species generation and cellular antioxidant status were determined for evaluating oxidative stress. For analyzing the effect of neferine on CoCl2-induced apoptosis, propidium iodide staining was performed. RESULTS: The results of the present study indicate that CoCl2 induces cell death in a dose-dependent manner. Neferine pretreatment at 700 nM concentration offers better cytoprotection in the cells exposed to CoCl2. Lactate dehydrogenase and NO release in the culture medium were restored after neferine pretreatment. CoCl2 triggers time-dependent reactive oxygen species generation in muscle cells. Further, results of propidium iodide staining, mitochondrial membrane potential, and intracellular calcium accumulation confirm that neferine offers protection against CoCl2-induced hypoxic injury. Depleted activities of antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, and glutathione S-transferase due to CoCl2 exposure were also reinstated in the group that received neferine pretreatment. CONCLUSION: Our study suggests that neferine from N. nucifera offers protection to muscle cells by counteracting the oxidative stress induced by CoCl2.