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Holzer P, Farzi A. Neuropeptides and the microbiota-gut-brain axis. Adv Exp Med Biol. 2014;817:195-219.

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Neuroprotective Effects of Cerebroprotein Hydrolysate on MPTP-induced Parkinson's Mice by Increasing Neurotrophin and Regulating Intestinal Microbiota

1Institute of Cerebrovascular Diseases, the Affiliated Hospital of Qingdao University, Qingdao 266003, China

2Shandong Provincial Collaborative Innovation Center for Neurodegenerative Disorders, Taishan Scholars Construction Project Excellent Innovative Team of Shandong Province, Qingdao 266003, China

3Department of Neurology,Shandong Second Provincial General Hospital,Jinan 250021

4Institute of Chinese integrative Medicine, Hebei Medical University, Shijiazhuang 050017, China.

5Songshan Hospital of Medical College, Qingdao University, Qingdao 266021, China


Journal of Food and Nutrition Research. 2023, Vol. 11 No. 8, 533-539
DOI: 10.12691/jfnr-11-8-3
Copyright © 2023 Science and Education Publishing

Cite this paper:
Yingjuan Liu, Yuqian Ren, Qinghua Zhang, Leiming Ren, Guanxi Wang. Neuroprotective Effects of Cerebroprotein Hydrolysate on MPTP-induced Parkinson's Mice by Increasing Neurotrophin and Regulating Intestinal Microbiota. Journal of Food and Nutrition Research. 2023; 11(8):533-539. doi: 10.12691/jfnr-11-8-3.

Correspondence to: Guanxi  Wang, Institute of Cerebrovascular Diseases, the Affiliated Hospital of Qingdao University, Qingdao 266003, China. Email: wangguanxi@163.com

Abstract

It is hypothesized that the neurotrophin loss and the intestinal tract could be a contributing factor to the neurodegenerative processes. Cerebroprotein hydrolysate-Ⅰ (CH-I), a mixture of amino acids and low molecular peptides had been reported to show remarkable therapeutic effect on many neurological diseases. However, the reports about the effects of cerebroprotein hydrolysate on PD was little. In this study, we applied CH-I on MPTP-induced mice to detect the neuroprotective effects. The results showed that CH-I could enhance the expression of neurotrophin (NGF and BDNF) and improve the behavioral deficits in MPTP-induced Parkinson's mice. Furthermore, CH-I restored the level of tyrosine hydroxylase (TH), and inhibited the apoptosis induced by MPTP. In addition, CH-I made a contribution to reducing the abundance of pathogenic microbiota and increasing the relative abundance of beneficial bacteria. The data demonstrate that CH-I shows promise as a novel treatment of PD.

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