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Evid Based Complement Alternat Med. 2019 Jan 08;2019:7276407. doi: 10.1155/2019/7276407. eCollection 2019.

Pilose Antler Extracts (PAEs) Protect against Neurodegeneration in 6-OHDA-Induced Parkinson's Disease Rat Models.

Evidence-based complementary and alternative medicine : eCAM

Chaohua Li, Yanan Sun, Weifeng Yang, Shuhua Ma, Lili Zhang, Jing Zhao, Xin Zhao, Yi Wang

Affiliations

  1. Xiyuan Hospital, China Academy of Chinese Medical Sciences, No. 1 Xiyuan Playground, Haidian District, Beijing 100091, China.
  2. Experimental Research Center, China Academy of Chinese Medical Sciences, No. 16, Nanxiao Road, Dongzhimen, Beijing 100700, China.
  3. School of Traditional Chinese Medicine, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenhe District, Shenyang, Liaoning Province 110016, China.
  4. School of Chinese Medicinal Materials, Jilin Agricultural University, No. 2888 Xincheng Avenue, Changchun City, Jilin Province 130118, China.

PMID: 30728849 PMCID: PMC6341246 DOI: 10.1155/2019/7276407

Abstract

Parkinson's disease (PD) is one of the most common neurodegenerative diseases worldwide. Although dopamine replacement therapy mitigates motor dysfunction in PD patients, there are no therapeutics that are currently available to reverse neuronal cell death in the substantia nigra pars compacta (SNc), which is the main region for dopamine loss in PD patients. The protein concentration of the Pilose antler extracts (PAEs) was estimated using the Bradford Protein Assay Kit. Hematoxylin and eosin (HE) staining was used to evaluate the protective effect of PAEs on 6-OHDA induced cell death in PD model rats. Immunohistochemistry (IHC) was used to detect the tyrosine hydroxylase (TH) positive neuronal cell in SNc. HPLC-MS was used to detect dopamine (DA), 3,4-Dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 5-hydroxytryptamine (5-HT), 5-hydroxyindoleacetic acid (5-HIAA), and glutamate (Glu) levels in the striatum and cerebrospinal fluid (CSF). The amino acid level in the striatum and CSF was measured by HPLC-FLD. Protein expression of growth associated protein-43 (GAP-43) and neurofilament heavy polypeptide (NF-H) was measured using western blotting. The components of PAEs through blood vessels were detected by HPLC/MS/MS. In this study, PAEs with proteins ranging from 10 kDa to 250 kDa molecular weight was administered to 6-OHDA-induced PD rats. We found that PAEs inhibited 6-OHDA-induced neuronal cell death and TH-positive neuronal loss in SNc. PAEs administration also increased the levels of DA, DOPAC, and 5-HT, in addition to DOPAC/DA and HVA/DA indexes in the CSF and Striatum of 6-OHDA induced rats. Conversely, PAEs decreased the levels of Glu and GABA. Treatment with PAEs and Madopar increased GAP-43 and NF-H expression in the SNc and striatum. Proteomic analysis using LC/MS/MS indicated that 11 components of PAEs may have neuropharmacological effects. These results demonstrate that PAEs protects against 6-OHDA induced toxic effects in the PD rat models. Intragastric administration of PAEs may be a novel therapeutic strategy for neurodegenerative disorders like PD.

References

  1. Int J Dev Biol. 2000;44(6):725-31 - PubMed
  2. J Comp Neurol. 2000 Dec 11;428(2):294-304 - PubMed
  3. Prog Brain Res. 2000;125:317-26 - PubMed
  4. Matrix Biol. 2001 Jul;20(4):215-31 - PubMed
  5. Exp Cell Res. 2005 Sep 10;309(1):185-97 - PubMed
  6. FASEB J. 2006 Apr;20(6):670-82 - PubMed
  7. J Neurochem. 2007 Oct;103(2):694-705 - PubMed
  8. Curr Opin Chem Biol. 2008 Jun;12(3):318-23 - PubMed
  9. Expert Opin Drug Deliv. 2010 Feb;7(2):203-24 - PubMed
  10. Expert Opin Pharmacother. 2010 Mar;11(4):627-35 - PubMed
  11. Parkinsonism Relat Disord. 2011 Sep;17(8):593-8 - PubMed
  12. Mol Biol Cell. 2012 Feb;23(4):553-66 - PubMed
  13. Yao Xue Xue Bao. 2011 Dec;46(12):1526-9 - PubMed
  14. Mol Psychiatry. 2013 Apr;18(4):425-34 - PubMed
  15. Mol Neurobiol. 2014 Aug;50(1):177-85 - PubMed
  16. Mol Neurobiol. 2016 Sep;53(7):4582-95 - PubMed
  17. Neurosci Lett. 2017 Sep 14;657:45-52 - PubMed
  18. Mol Med Rep. 2017 Oct;16(4):5143-5150 - PubMed
  19. Br Med J (Clin Res Ed). 1981 Apr 11;282(6271):1239 - PubMed
  20. JAMA. 1999 Jan 27;281(4):341-6 - PubMed

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