Abstract Title:

Annatto prevents retinal degeneration induced by endoplasmic reticulum stress in vitro and in vivo.

Abstract Source:

Mol Nutr Food Res. 2012 May ;56(5):713-24. PMID: 22648618

Abstract Author(s):

Kazuhiro Tsuruma, Hiroki Shimazaki, Ken-Ichi Nakashima, Mika Yamauchi, Sou Sugitani, Masamitsu Shimazawa, Munekazu Iinuma, Hideaki Hara

Article Affiliation:

Kazuhiro Tsuruma


SCOPE: Annatto (Bixa orellana) seeds have been used as a colorant in butter and in a variety of other foods. In this study, we investigated the amelioration of retinal damage by an acetone extract of annatto (A-ext.), bixin (a main component of annatto), and four bixin derivatives (Bx-1, Bx-2, Bx-3, and Bx-4) that we have synthesized.

METHODS AND RESULTS: We used cultured retinal ganglion cells (RGC-5) to examine in vitro effects of A-ext. on stress pathways, focusing on intracellular oxidation induced by reactive oxygen species, expression of endoplasmic reticulum (ER) stress-related proteins, caspase-3 activation, and cell membrane damage. In vivo retinal damage in mice following intravitreous injection of tunicamycin was evaluated by counting the cell numbers in the ganglion cell layer (GCL) and measuring the thickness of outer nuclear layer (ONL). A-ext., bixin, and Bx-1 treatment inhibited both tunicamycin- and H₂O₂-induced cell death. Bixin derivatives also inhibited tunicamycin-induced cell death. Treatment with A-ext., bixin, and Bx-1 reduced tunicamycin-induced caspase-3 activity and inhibited the inversion of phosphatidylserine, an early apoptotic event without antioxidant effect or reduction of ERstress itself. A-ext., bixin, and Bx-1 significantly inhibited the tunicamycin-induced loss of cells from the GCL, and these materials also suppressed the tunicamycin-induced thinning of ONL.

CONCLUSION: A-ext., its main component bixin, and bixin derivatives may therefore be useful for preventive and therapeutic treatment of retinal-related diseases.

Study Type : Animal Study, In Vitro Study
Additional Links
Pharmacological Actions : Anti-Apoptotic : CK(2905) : AC(1672)

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