73 research outputs found

    Natural flavonoids as potential multifunctional agents in prevention of diabetic cataract

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    Cataract is one of the earliest secondary complications of diabetes mellitus. The lens is a closed system with limited capability to repair or regenerate itself. Current evidence supports the view that cataractogenesis is a multifactorial process. Mechanisms related to glucose toxicity, namely oxidative stress, processes of non-enzymatic glycation and enhanced polyol pathway significantly contribute to the development of eye lens opacity under conditions of diabetes. There is an urgent need for inexpensive, non-surgical approaches to the treatment of cataract. Recently, considerable attention has been devoted to the search for phytochemical therapeutics. Several pharmacological actions of natural flavonoids may operate in the prevention of cataract since flavonoids are capable of affecting multiple mechanisms or etiological factors responsible for the development of diabetic cataract. In the present paper, natural flavonoids are reviewed as potential agents that could reduce the risk of cataract formation via affecting multiple pathways pertinent to eye lens opacification. In addition, the bioavailability of flavonoids for the lens is considered

    Ex vivo effects of vegetables as ingredient on the antioxidant activity of miso soup

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    Neurotrophic factor-like effect of FPF1070 on septal cholinergic neurons after transections of fimbria-fornix in the rat brain

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    FPF1070 is an aqueous protein-free solution, which consists of 85% free amino acids and 15% small peptides. Our previous study showed a potent neurotrophic factor-like activity in cultured embryonic cells of dorsal root ganglia. The present study investigated whether FPF1070 regenerated the cholinergic cells in the media1 septal nucleus after axonal transections by cutting the fimbria-fornix. Fimbrial transections reduced the number of septal cholinergic cells by 30 + 3.6%, compared with the number on contralateral sides at 4 weeks. Intrapretioneal injections of FPF1070 caused 49.9 * 6.3% of the cholinergic neurons to survive. Furthermore, the cell sizes of the cholinergic neurons were significantly different: 16.4 + 4.2 pm, 14.3 I3. 8 pm in FPF1070 treatment and vehicle treatment, respectively. These results indicated that FPF1070 prevents the degeneration and atrophy of impaired cholinergic neurons by systemic administration
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