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Research Paper|Volume 11, Issue 4|pp 1177—1188

Nutraceutical effects of Emblica officinalis in age-related macular degeneration

Sonali Nashine1, Raj Kanodia2, Anthony B. Nesburn1,3, Girish Soman4, Baruch D. Kuppermann1, M. Cristina Kenney1,5
  • 1Department of Ophthalmology, Gavin Herbert Eye Institute, University of California Irvine, Irvine, CA 92697, USA
  • 2Rhinoplasty Surgeon, Dr. Raj Kanodia Medical Group, Beverly Hills, CA 90210, USA
  • 3Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA
  • 4Nisarga Biotech Pvt Ltd, Janai Malai, Satara, Maharashtra, 415004, India
  • 5Department of Pathology and Laboratory Medicine, University of California Irvine, Irvine, CA 92697, USA
Received: December 26, 2018Accepted: February 6, 2019Published: February 21, 2019
https://doi.org/10.18632/aging.101820

Copyright: © 2019 Nashine et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Emblica officinalis Gaetrn (i.e., Phyllanthus emblica/ Indian gooseberry/ Amla) (EO) has been used extensively as a nutraceutical in several diseases since it is known to boost immunity and offers numerous health benefits such as antioxidant, anti-inflammatory, and anti-aging effects. The goal of our study was to test the hypothesis that EO will rescue human AMD RPE transmitochondrial cells from mitochondria-induced cellular damage. AMD RPE transmitochondrial cell lines were created by fusion of mitochondria DNA-deficient APRE-19 (Rho0) cells with platelets isolated from AMD patients, and therefore had identical nuclei but differed in mitochondrial DNA content. These AMD RPE cells were treated with EO extract followed by characterization of effects of EO using cellular and molecular assays. Herein, EO significantly improved live cell number and mitochondrial membrane potential, reduced apoptosis and oxidative stress, down-regulated VEGF, and up-regulated PGC-1α. In conclusion, EO improved cellular and mitochondrial health, thereby playing a key cytoprotective role in AMD in vitro. Further studies are required to examine the mechanisms that mediate the cytoprotective effects of EO.