Antioxidant and antibacterial effects of medicinal plants and their stick-type medicinal concentrated beverages.

Nine medicinal plants and their stick-type medicinal concentrated beverages (SMCB-I and SMCB-II) with different combination ratio were evaluated on antioxidant, nitric oxide (NO) inhibitory, and antibacterial effects against pathogenic bacteria involved in respiratory system illnesses. Antioxidant activity was high in Syzygium aromaticum, Pueraria lobata, Plantago asiatica, and Kalopanax pictus which have higher contents of total phenolics and total flavonoids. The NO inhibitory activity was high in Syzygium aromaticum, Plantago asiatica, and Glycyrrhiza uralensis. Syzygium aromaticum, Plantago asiatica, Kalopanax pictus and Glycyrrhiza uralensis showed higher antibacterial activity than the other five medicinal plants against Staphylococcus aureus, Corynebacterium diphtheriae, and Mycobacterium sp. SMCB-II exhibited higher antioxidant, NO inhibitory, and antibacterial effects than SMCB-I, since Syzygium aromaticum, Pueraria lobata, and Kalopanax pictus were only used for the production of SMCB-II. The SMCBs would be expected to contribute to an easy-to-carry, easy-to-consume, and high value-added health beverage for the modern people.

De Novo Shoot Regeneration Controlled by HEN1 and TCP3/4 in Arabidopsis.

Plants have the ability to regenerate whole plant body parts, including shoots and roots, in vitro from callus derived from a variety of tissues. However, the underlying mechanisms for this de novo organogenesis, which is based on the totipotency of callus cells, are poorly understood. Here, we report that a microRNA (miRNA)-mediated posttranscriptional regulation plays an important role in de novo shoot regeneration. We found that mutations in HUA ENHANCER 1 (HEN1), a gene encoding a small RNA methyltransferase, cause cytokinin-related defects in de novo shoot regeneration. A hen1 mutation caused a large reduction in the miRNA319 (miR319) level and a subsequent increase in its known target (TCP3 and TCP4) transcript levels. TCP transcription factors redundantly inhibited shoot regeneration and directly activated the expression of a negative regulator of cytokinin response ARABIDOPSIS THALIANA RESPONSE REGULATOR 16 (ARR16). A tcp4 mutation at least partly rescued the shoot-regeneration defect and derepression of ARR16 in hen1. These findings demonstrate that the miR319-TCP3/4-ARR16 axis controls de novo shoot regeneration by modulating cytokinin responses.