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Leaves of Persimmon (Diospyros kaki Thunb.) Ameliorate N-Methyl-N-nitrosourea (MNU)-Induced Retinal Degeneration in Mice.

Abstract
The purpose of the study was to investigate the protective effects of the ethanol extract of Diospyros kaki (EEDK) persimmon leaves to study N-methyl-N-nitrosourea (MNU)-induced retinal degeneration in mice. EEDK was orally administered after MNU injection. Retinal layer thicknesses were significantly increased in the EEDK-treated group compared with the MNU-treated group. The outer nuclear layer was preserved in the retinas of EEDK-treated mice. Moreover, EEDK treatment reduced the MNU-dependent up-regulation of glial fibrillary acidic protein (GFAP) and nestin expression in Müller and astrocyte cells. EEDK treatment also inhibited MNU-dependent down-regulation of rhodopsin expression. Quercetin exposure significantly attenuated the negative effects of H2O2 in R28 cells, suggesting that quercetin can act in an antioxidative capacity. Thus, EEDK may be considered as an agent for treating or preventing degenerative retinal diseases, such as retinitis pigmentosa and age-related macular degeneration.
AuthorsKyung-A Kim, Suk Woo Kang, Hong Ryul Ahn, Youngwoo Song, Sung Jae Yang, Sang Hoon Jung
JournalJournal of agricultural and food chemistry (J Agric Food Chem) Vol. 63 Issue 35 Pg. 7750-9 (Sep 09 2015) ISSN: 1520-5118 [Electronic] United States
PMID26260943 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Glial Fibrillary Acidic Protein
  • Nerve Tissue Proteins
  • Nes protein, mouse
  • Nestin
  • Plant Extracts
  • glial fibrillary astrocytic protein, mouse
  • Methylnitrosourea
Topics
  • Animals
  • Diospyros (chemistry)
  • Disease Models, Animal
  • Glial Fibrillary Acidic Protein
  • Humans
  • Male
  • Methylnitrosourea (adverse effects)
  • Mice
  • Mice, Inbred C57BL
  • Nerve Tissue Proteins (genetics, metabolism)
  • Nestin (genetics, metabolism)
  • Plant Extracts (administration & dosage)
  • Plant Leaves (chemistry)
  • Retinal Degeneration (chemically induced, drug therapy, genetics, metabolism)

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