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Abstract

Neuroprotective Potential of Cranberry Juice against Parkinson’s Disease †

by
Monika Kurpik
1,
Łukasz Witucki
2,
Jadwiga Jodynis-Liebert
1 and
Małgorzata Kujawska
1,*
1
Department of Toxicology, Poznan University of Medical Sciences, Dojazd 30, 60-631 Poznan, Poland
2
Department of Biochemistry and Biotechnology, Poznan University of Life Sciences, Dojazd 11, 60-632 Poznan, Poland
*
Author to whom correspondence should be addressed.
Presented at the 2nd International Electronic Conference on Brain Sciences, 15–30 July 2021. Available online: https://sciforum.net/event/IECBS2021.
Med. Sci. Forum 2022, 8(1), 5; https://doi.org/10.3390/IECBS2021-10673
Published: 5 July 2022
(This article belongs to the Proceedings of The 2nd International Electronic Conference on Brain Sciences)

Abstract

:
Parkinson’s disease (PD) is a neurodegenerative disorder characterized by motor dysfunction associated with a loss of dopaminergic (DAergic) neurons in the substantia nigra pars compacta (SNpc) and the presence of Lewy bodies, mainly composed of aggregated α-synuclein (ASN), in the brain [1]. Cranberry juice (CJ) is a rich source of polyphenols with strong antioxidant activity, which is believed to contribute to this fruit’s wide range of health benefits. However, to date, our knowledge of cranberry neuroprotective potential is very scarce and limited to only a few in vitro studies. Recently, we have reported that treatment with CJ controls oxidative stress in several organs, with the most noticeable effect occurring in the brain [2]. It has been shown that rats exposed to prolonged low-dose of rotenone (ROT) treatment develop PD-like neurodegeneration due to complex I inhibition and associated oxidative damage, ASN aggregation, and loss of DAergic neurons in the SNpc [3]. This study aimed to examine CJ’s ability to modulate the apoptosis mechanism and thereby provide neuroprotection in an ROT-induced rat model of parkinsonism. Wistar rats were given treatment with CJ in a dose of 500 mg/kg b.w./day (i.g.) and injected with ROT (1.3 mg/kg b.w./day, s.c.) from the 11th day. The experiment lasted a total of 45 days, including 10 days pre-treatment with CJ and 35 days combined treatment with CJ and ROT. To evaluate its neuroprotective effect, a microscopic examination, determination of inflammation and apoptosis markers, and ASN level were performed in the midbrain. Our results indicated that the CJ treatment provided neuroprotection, as evidenced by an enhancement of neuronal survival, which correlated well with the decreased expression of pro-apoptotic caspase-9 and Bax and normalization of cytochrome c levels. Importantly, treatment with CJ declined α-synuclein levels. The expression of tumor necrosis factor-alpha (TNF-α) was similar across all groups, with no statistically significant differences.

Supplementary Materials

The following are available online at https://www.mdpi.com/article/10.3390/IECBS2021-10673/s1, Figure S1: Apoptosis marker and α-synuclein, Figure S2: Representative photomicrographs (* 40) of H&E stained midbrain sections of rats.

Author Contributions

Methodology, Ł.W, and M.K. (Małgorzata Kujawska); software, M.K. (Małgorzata Kujawska), and Ł.W.; formal analysis, M.K. (Małgorzata Kujawska) and Ł.W.; investigation, Ł.W., and M.K. (Monika Kurpik); resources, M.K. (Małgorzata Kujawska), Ł.W, and J.J.-L.; data curation, Ł.W. and M.K. (Małgorzata Kujawska); writing—original draft preparation, M.K. (Małgorzata Kujawska); writing—review and editing, M.K. (Małgorzata Kujawska), Ł.W. and J.J.-L.; visualization, Ł.W.; supervision, M.K. (Małgorzata Kujawska) and J.J.-L.; project administration, M.K. (Małgorzata Kujawska) and J.J.-L.; funding acquisition M.K. (Małgorzata Kujawska). All authors have read and agreed to the published version of the manuscript.

Funding

This research was funded by Narodowe Centrum Nauki, grant ID 2017/26/D/NZ7/00748.

Institutional Review Board Statement

The experiment was performed in accordance with Polish governmental regulations (Dz. U. 05.33.289) and with EU Directive 2010/63/EU for animal experiments. The study protocol was approved by the Local Ethics Committee on the Use of Laboratory Animals in Poznań, Poland (58/2016, 7 October 2016).

Informed Consent Statement

Not applicable.

Data Availability Statement

Original data are available with the authors according to their contribution but not archived in databases elsewhere.

Conflicts of Interest

The authors declare no conflict of interest.

References

  1. Kalia, L.V.; Lang, A.E. Parkinson’s disease. Lancet 2015, 386, 896–912. [Google Scholar] [CrossRef]
  2. Kurpik, M.; Zalewski, P.; Kujawska, M.; Ewertowska, M.; Ignatowicz, E.; Cielecka-Piontek, J.; Jodynis-Liebert, J. Can Cranberry uice Protect against Rotenone-Induced Toxicity in Rats? Nutrients 2021, 13, 1050. [Google Scholar] [CrossRef] [PubMed]
  3. Kujawska, M.; Jourdes, M.; Kurpik, M.; Szulc, M.; Szaefer, H.; Chmielarz, P.; Kreiner, G.; Krajka-Kuźniak, V.; Mikołajczak, P.; Teissedre, P.L.; et al. Neuroprotective Effects of Pomegranate Juice against Parkinson’s Disease and Presence of Ellagitannins-Derived Metabolite-Urolithin A-In the Brain. Int. J. Mol. Sci. 2019, 21, 202. [Google Scholar] [CrossRef] [PubMed] [Green Version]
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MDPI and ACS Style

Kurpik, M.; Witucki, Ł.; Jodynis-Liebert, J.; Kujawska, M. Neuroprotective Potential of Cranberry Juice against Parkinson’s Disease. Med. Sci. Forum 2022, 8, 5. https://doi.org/10.3390/IECBS2021-10673

AMA Style

Kurpik M, Witucki Ł, Jodynis-Liebert J, Kujawska M. Neuroprotective Potential of Cranberry Juice against Parkinson’s Disease. Medical Sciences Forum. 2022; 8(1):5. https://doi.org/10.3390/IECBS2021-10673

Chicago/Turabian Style

Kurpik, Monika, Łukasz Witucki, Jadwiga Jodynis-Liebert, and Małgorzata Kujawska. 2022. "Neuroprotective Potential of Cranberry Juice against Parkinson’s Disease" Medical Sciences Forum 8, no. 1: 5. https://doi.org/10.3390/IECBS2021-10673

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