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Int J Mol Sci. 2019 Dec 27;21(1). pii: E202. doi: 10.3390/ijms21010202.

Neuroprotective Effects of Pomegranate Juice against Parkinson's Disease and Presence of Ellagitannins-Derived Metabolite-Urolithin A-In the Brain.

Author information

1
Department of Toxicology, Poznan University of Medical Sciences, Dojazd 30, 60-631 Poznań, Poland.
2
Université de Bordeaux, ISVV, EA 4577, Œnologie, 210 Chemin de Leysotte, F-33140 Villenave d'Ornon, France.
3
INRA, ISVV, USC 1366 INRA, IPB, 210 Chemin de Leysotte, F-33140 Villenave d'Ornon, France.
4
Department of Pharmacology, Poznan University of Medical Sciences, Rokietnicka 5a, 60-806 Poznan, Poland.
5
Department of Pharmaceutical Biochemistry, Poznan University of Medical Sciences, Święcickiego 4, 60-781 Poznań, Poland.
6
Department of Brain Biochemistry, Maj Institute of Pharmacology, Polish Academy of Sciences, Smętna 12, 31-343 Kraków, Poland.

Abstract

Pomegranate juice is a rich source of ellagitannins (ETs) believed to contribute to a wide range of pomegranate's health benefits. While a lot of experimental studies have been devoted to Alzheimer disease and hypoxic-ischemic brain injury, our knowledge of pomegranate's effects against Parkinson's disease (PD) is very limited. It is suggested that its neuroprotective effects are mediated by ETs-derived metabolites-urolithins. In this study, we examined the capability of pomegranate juice for protection against PD in a rat model of parkinsonism induced by rotenone. To evaluate its efficiency, assessment of postural instability, visualization of neurodegeneration, determination of oxidative damage to lipids and α-synuclein level, as well as markers of antioxidant defense status, inflammation, and apoptosis, were performed in the midbrain. We also check the presence of plausible active pomegranate ETs-derived metabolite, urolithin A, in the plasma and brain. Our results indicated that pomegranate juice treatment provided neuroprotection as evidenced by the postural stability improvement, enhancement of neuronal survival, its protection against oxidative damage and α-synuclein aggregation, the increase in mitochondrial aldehyde dehydrogenase activity, and maintenance of antiapoptotic Bcl-xL protein at the control level. In addition, we have provided evidence for the distribution of urolithin A to the brain.

KEYWORDS:

antioxidant enzymes; apoptosis; ellagic acid; ellagitannins; mitochondrial aldehyde dehydrogenase; neurodegeneration; pomegranate juice; rotenone; urolithin A

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