4.7 Article

Ameliorative effects of functional chalaza hydrolysates prepared from protease-A digestion on cognitive dysfunction and brain oxidative damages

Journal

POULTRY SCIENCE
Volume 99, Issue 5, Pages 2819-2832

Publisher

ELSEVIER
DOI: 10.1016/j.psj.2019.12.060

Keywords

antioxidant/anti-inflammatory capacity; crude chalaza hydrolysate; cognitive dysfunction; D-galactose; hippocampus morphology

Funding

  1. Ministry of Science and Technology, Taiwan [MOST 106-2313-B-002-040-MY3]

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Our patented protease A-digested crude chalaza hydrolysates (CCH) show antioxidant abilities in vitro. The prophylactic effects of CCH on cognitive dysfunction and brain oxidative damages were investigated via a D-galactose (DG)-injected mouse model in this study. Fifty-four mice were randomly divided into the following: (1) CON, 0.1 mL 0.9% saline (subcutaneous injection [SC] on the back)1distilled water (oral gavage); (2) DG, 100 mg/kg BW/day D-galactose (BioServ Co., Flemington, NJ, USA) (SC on the back)1 distilled water (oral gavage); (3) DG_LCH, 100 mg/kg BW/day D-galactose (SC on the back) 150 mg CCH/kg BW/day in 0.1 ml distilled water (oral gavage); (4) DG_MCH, 100 mg/kg BW/day D-galactose (SC on the back) 1 100 mg CCH/kg BW/day (oral gavage); (5) DG_HCH, 100 mg/kg BW/day D-galactose (SC on the back) 1 200 mg CCH/kg BW/day (oral gavage); (6) DG_AG, 100 mg/kg BW/day D-galactose (SC on the back) 1 100 mg aminoguanidine hydrochloride/kg BW/day (oral gavage). The experiment lasted for 84 D. CCH, containing antioxidant-free amino acids and anserine, restored (P< 0.05) DG-injected memory injury in the Morris water maze test and attenuated the neuronal degenerations and nucleus shrinkages in the dentate gyrus area. CCH supplementation also reduced amyloid beta-peptide protein levels and accumulation of advanced glycation end products (AGE) in the brain of DGinjected mice, whereas the brain antioxidant capacity was reversed (P< 0.05) by supplementing CCH. Furthermore, AGE receptor (RAGE), NF kappa b, IL-beta(,) and TNF-alpha gene expressions were downregulated (P < 0.05) by supplementing CCH. Therefore, CCH show prophylactic effects on the development of oxidative stressinduced cognitive dysfunction.

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