Background: Alzheimer's (AD) is one of the most common neurodegenerative diseases, causing dementia and brain cells death.
Objectives: This study aimed to assess the ameliorating effect of probiotic against AD induced in rats by d-galactose and AlCl injection via evaluating mitochondrial parameter changes in hippocampus.
Methods: This study was carried out on rats were classified into five groups; G1 (control group), G2 (probiotic group), G3 (AD group), G4 (co-treated group) and G5 (post-treated group). By the end of the experiment, some different neurotransmitters, oxidative stress biomarkers, zinc, blood glucose, NaKATPase subunit alpha 1 (ATP1A1), and gene expression of mitochondrial membrane potential (MMP) were measured.
Results: Significant changes in neurotransmitters, antioxidants levels and decreased ATP1A1 activity and gene expression of MMP in the hippocampus in G3 were detected if compared to control. Best improvement in G5 than G4 group was observed. These results were confirmed by histological and immunohistochemical studies in hippocampus.
Conclusions: Acidophilus probiotic was able to alleviate learning and memory associated injuries in AD by reducing mitochondrial dysfunction induced by d-galactose and AlCl. This may be associated with its antioxidant properties.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.1515/jcim-2020-0156 | DOI Listing |
Neuroscience
December 2024
Key Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu 610041, China. Electronic address:
In Vivo
October 2024
School of Pharmacy, Faculty of Pharmacy and Pharmaceutical Sciences, Josai University, Saitama, Japan;
Background/aim: Alzheimer's disease (AD) is the most common form of dementia worldwide. Nattokinase is a serine protease extracellularly produced by natto, a fermented product of Bacillus subtilis var. natto.
View Article and Find Full Text PDFHeliyon
October 2024
School of Pharmaceutical Sciences & Institute of Materia Medica, Shandong First Medical University & Shandong Academy of Medical Sciences, Jinan, 250117, China.
In this study we have investigated the effect of chondroitin sulfate-selenium nanoparticles (CS@Se) on Alzheimer's disease (AD) mice using 16S rDNA technique. We randomly divided 30 SPF grade male C57BL/6 J mice into 6 groups according to random number table method. The AD mouse model was established by subcutaneous injection of D-galactose (D-gal) combined with gavage of AlCl for 30 consecutive days, and then drug intervention was performed in the administration group for 40 consecutive days.
View Article and Find Full Text PDFACS Omega
October 2024
Department of Chemical Engineering (ENTEG), University of Groningen, Nijenborgh 4, Groningen, AG 9747, The Netherlands.
5-Hydroxymethylfurfural (HMF) is an attractive building block for biobased chemicals. Typically, ketoses like d-fructose (FRC) are suitable starting materials and give good yields of HMF in a simple aqueous phase process with a Bro̷nsted acid catalyst. With aldoses, such as d-glucose (GLU), much lower yields were reported in the literature.
View Article and Find Full Text PDFPhytomedicine
December 2024
College of Chinese Medicinal Materials, National & Local Joint Engineering Research Center for Ginseng Breeding and Development, Jilin Agricultural University, Changchun 130118, PR China; College of Life Sciences, Jilin Agricultural University, Changchun 130118, PR China. Electronic address:
Background: Damage to the blood-brain barrier (BBB) is vital for the development of Alzheimer's disease (AD). Ginsenoside Rg2 (G-Rg2) has been shown to improve a variety of brain injuries, but whether G-Rg2 can improve the BBB leakage related to AD is still unclear.
Purpose: Illuminate the effect and mechanism of G-Rg2 on AD-related BBB damage.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!