Dataset Information

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

ABSTRACT: 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)+distilled water (oral gavage); (2) DG, 100 mg/kg BW/day D-galactose (Bio-Serv Co., Flemington, NJ, USA) (SC on the back)+distilled water (oral gavage); (3) DG_LCH, 100 mg/kg BW/day D-galactose (SC on the back) + 50 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) + 100 mg CCH/kg BW/day (oral gavage); (5) DG_HCH, 100 mg/kg BW/day D-galactose (SC on the back) + 200 mg CCH/kg BW/day (oral gavage); (6) DG_AG, 100 mg/kg BW/day D-galactose (SC on the back) + 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 ?-peptide protein levels and accumulation of advanced glycation end products (AGE) in the brain of DG-injected mice, whereas the brain antioxidant capacity was reversed (P < 0.05) by supplementing CCH. Furthermore, AGE receptor (RAGE), NF?b, IL-6, and TNF-? gene expressions were downregulated (P < 0.05) by supplementing CCH. Therefore, CCH show prophylactic effects on the development of oxidative stress-induced cognitive dysfunction.

SUBMITTER: Chan CJ

PROVIDER: S-EPMC7597535 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

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

Chan Chia-Jung CJ Tseng Jung-Kai JK Wang Sheng-Yao SY Lin Yi-Ling YL Samuel Wu Yi-Hsieng YH Chen Jr-Wei JW Chen Yi-Chen YC

Poultry science 20200320 5

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)+distilled water (oral gavage); (2) DG, 100 mg/kg BW/day D-galactose (Bio-Serv Co., Flemington, NJ, USA) (SC ...[more]

PMID: 32359619

Similar Datasets

Project description:Neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), are multifactorial. Among various factors, lipopolysaccharides (LPSs) from Gram-negative bacteria, such as E. coli, are considered potential causative agents. Despite significant advancements in the field, there is still no cure. In this study, we investigated the neuroprotective effects of ambroxol against LPS-induced neuroinflammation, oxidative stress, neurodegeneration, and the associated cognitive dysfunction. Intraperitoneal injection of LPS (250 µg/kg every alternative day for a total of seven doses over 14 days) triggered glial cell activation, neuroinflammation, oxidative stress, and neurodegeneration in the mouse brain. Ambroxol treatment (30 mg/kg/day for 14 days) significantly reduced neuroinflammation and oxidative stress compared to LPS-treated mice. Immunoblotting and immunofluorescence results showed that ambroxol reduced levels of Toll-like receptor 4 (TLR4) and oxidative stress kinase phospho-c-Jun N-terminal Kinase 1 (p-JNK). It also decreased astrocyte and microglia activation in the cortex and hippocampus of LPS+ Amb-treated mice, as indicated by the downregulation of GFAP and Iba-1. Furthermore, ambroxol-reversed LPS-induced neuroinflammation by inhibiting inflammatory mediators, such as IL-1β and TNF-α, through regulation of the transcription factor p-NFkB. Persistent neuroinflammation disrupted the natural antioxidant mechanisms, leading to oxidative stress. Ambroxol treatment upregulated antioxidant markers, including Nrf-2, HO-1, and SOD, which were downregulated in the LPS-treated group. Additionally, ambroxol-inhibited lipid peroxidation, maintaining malondialdehyde levels in the mouse brain. Ambroxol also improves synaptic integrity by upregulating synaptic biomarkers, including PSD-95 and SNAP-23. Overall, ambroxol demonstrated anti-inflammatory, antioxidant, and neuroprotective effects in LPS-treated mice, highlighting its potential benefits in neurological disorders.

Dataset Information

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

Publications

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

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets