scholarly journals An Examination of Lactobacillus paracasei GKS6 and Bifidobacterium lactis GKK2 Isolated from Infant Feces in an Aged Mouse Model

2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Shih-Wei Lin ◽  
You-Shan Tsai ◽  
Yen-Lien Chen ◽  
Ming-Fu Wang ◽  
Chin-Chu Chen ◽  
...  
Keyword(s):  
Population Aging ◽  
Thiobarbituric Acid ◽  
Lactobacillus Paracasei ◽  
Aged Mouse ◽  
Bifidobacterium Lactis ◽  
Age Related ◽  
Fiber Number ◽  
Infant Feces ◽  
Muscle Fiber Number ◽  
Samp8 Mice

Supplementary which could maintain normal physiological mechanisms and functions while aging has drawn our attention due to the population aging in recent years. Probiotics have been believed with desirable properties such as antioxidation and anti-inflammatory for delaying the aging process. However, the age-related experiments conducted in the mammalian models with probiotics were few. In this study, we demonstrated the effects of administration of probiotics Lactobacillus paracasei GKS6 (GKS6) and Bifidobacterium lactis GKK2 (GKK2), respectively, at the dosage of 5.0 × 109 cfu/kg BW/day for fourteen weeks in senescence-accelerated mouse prone 8 (SAMP8) mice. The three-month-old SAMP8 mice were divided into three groups: control, mice fed with GKS6, and mice fed with GKK2. There were ten females and ten males in each group. The SAMP8 mice fed with probiotics GKS6 and GKK2 showed a significantly lower degree of aging followed by Takeda’s grading method on the eleventh week of the experiment. The GKK2 group showed significantly increased forelimb grip strength in male SAMP8 mice and muscle fiber number in both genders. Compared to the control, both GKS6 and GKK2 presented a significant increase in liver superoxide dismutase and catalase activities. In addition, a significant decrease in the levels of liver thiobarbituric acid-reactive substances was observed in the probiotics group. These results suggested that probiotics GKS6 and GKK2 could act as antioxidants in delaying the process of aging and preventing age-related muscle loss.

scholarly journals Lactobacillus paracasei PS23 decelerated age-related muscle loss by ensuring mitochondrial function in SAMP8 mice

Aging ◽  
2019 ◽  
Vol 11 (2) ◽  
pp. 756-770 ◽  
Author(s):  
Li-Han Chen ◽  
Shih-Yi Huang ◽  
Kuo-Chin Huang ◽  
Chih-Chieh Hsu ◽  
Kuen-Cheh Yang ◽  
...  
Keyword(s):  
Mitochondrial Function ◽  
Lactobacillus Paracasei ◽  
Muscle Loss ◽  
Age Related ◽  
Samp8 Mice

scholarly journals Lactobacillus paracasei PS23 Delays Progression of Age-Related Cognitive Decline in Senescence Accelerated Mouse Prone 8 (SAMP8) Mice

Nutrients ◽  
2018 ◽  
Vol 10 (7) ◽  
pp. 894 ◽  
Author(s):  
Shih-Yi Huang ◽  
Li-Han Chen ◽  
Ming-Fu Wang ◽  
Chih-Chieh Hsu ◽  
Ching-Hung Chan ◽  
...  
Keyword(s):  
Cognitive Decline ◽  
Brain Dysfunction ◽  
Lactobacillus Paracasei ◽  
Oxidative Enzymes ◽  
Control Group ◽  
Age Related ◽  
Chemotactic Protein ◽  
Age Related Cognitive Decline ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse

Probiotic supplements are potential therapeutic agents for age-related disorders due to their antioxidant and anti-inflammatory properties. However, the effect of probiotics on age-related brain dysfunction remains unclear. To investigate the effects of Lactobacillus paracasei PS23 (LPPS23) on the progression of age-related cognitive decline, male and female senescence-accelerated mouse prone 8 (SAMP8) mice were divided into two groups (n = 6 each): the control and PS23 groups. From the age of 16 weeks, these groups were given saline and LPPS23, respectively, because SAMP8 mice start aging rapidly after four months of age. After 12 weeks of treatment, we evaluated the effect of LPPS23 by analyzing their appearance, behavior, neural monoamines, anti-oxidative enzymes, and inflammatory cytokines. The PS23 group showed lower scores of senescence and less serious anxiety-like behaviors and memory impairment compared to the control group. The control mice also showed lower levels of neural monoamines in the striatum, hippocampus, and serum. Moreover, LPPS23 induced the anti-oxidative enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPx). Higher levels of tumor necrosis factor (TNF)-α and monocyte chemotactic protein-1 (MCP1) and lower levels of interleukin (IL)-10 indicated that LPPS23 modulated the inflammation. Our results suggest that LPPS23 supplements could delay age-related cognitive decline, possibly by preventing oxidation and inflammation and modulating gut–brain axis communication.

scholarly journals Lactobacillus paracasei PS23 modulated the age‐related inflammation in Senescence Accelerated Mouse Prone 8 (SAMP8) mice

2019 ◽  
Vol 33 (S1) ◽  
Author(s):  
Hui‐Yu Huang ◽  
Ying‐Xu Huang ◽  
Yi‐Wen Chen ◽  
Nien‐Wei Chou ◽  
Yi‐Rong Chen ◽  
...  
Keyword(s):  
Lactobacillus Paracasei ◽  
Age Related ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse

scholarly journals Metformin protects lens epithelial cells against senescence in a naturally aged mouse model

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Mengmeng Chen ◽  
Yushan Fu ◽  
Xu Wang ◽  
Ruitong Wu ◽  
Dongmei Su ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Vision Loss ◽  
Adenosine Monophosphate ◽  
Underlying Mechanism ◽  
Ageing Process ◽  
Lens Epithelial Cells ◽  
Control Group ◽  
Aged Mouse ◽  
Ampk Pathway ◽  
Age Related

AbstractThe senescence of lens epithelial cells (LECs) is a major factor leading to age-related cataract (ARC). ARC results in visual impairment and severe vision loss in elderly patients. However, the specific mechanism of ARC remains unclear, and there are no effective therapeutic agents to halt the formation of ARC. This study aimed to assess the underlying mechanism of the formation of ARC and investigate the potential anti-ageing effect of metformin (MET) on ARC. Male C57BL/6 mice were divided into three groups: the control group having young mice (3 months old, n = 40), the naturally aged group (aged 20 months, n = 60) and the MET group (MET, 20 months, n = 60). Mice in the control and the naturally aged groups were fed a standard purified mouse diet ad libitum and water, whereas those in the MET group were fed chows supplemented with 0.1% MET for 10 months. The transparency of the lens and age-associated proteins p21 and p53 were analysed in the LECs of these three groups. Furthermore, we determined the expressions of the adenosine monophosphate (AMP)-activated protein kinase (AMPK) pathway and the effect of MET on this pathway in LECs during the ageing process of ARC. In addition, the relationship between autophagy and the senescence of LECs and the role of MET in the autophagy of LECs during the ageing process of ARC were examined. Our results indicated that age-related inactivation of the AMPK pathway and impairment of autophagy might contribute to the senescence of LECs and the occurrence of ARC. More importantly, these results demonstrated that MET effectively alleviated the senescence of LECs and the formation of ARC probably via inactivation of the AMPK pathway and augmentation of autophagy. These findings revealed that MET can be exploited as a potentially useful drug for ARC prevention. Our study will help in enlightening the development of innovative strategies for the clinical treatment of ARC.

scholarly journals Inhibition of 11β-HSD1 Ameliorates Cognition and Molecular Detrimental Changes after Chronic Mild Stress in SAMP8 Mice

2021 ◽  
Vol 14 (10) ◽  
pp. 1040
Author(s):  
Dolors Puigoriol-Illamola ◽  
Júlia Companys-Alemany ◽  
Kris McGuire ◽  
Natalie Z. M. Homer ◽  
Rosana Leiva ◽  
...  
Keyword(s):  
Stress Responses ◽  
Healthy Aging ◽  
Molecular Mechanisms ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Cognitive Improvement ◽  
Age Related ◽  
Mtorc1 Signaling ◽  
Cognitive Disturbances ◽  
Samp8 Mice

Impaired glucocorticoid (GC) signaling is a significant factor in aging, stress, and neurodegenerative diseases such as Alzheimer’s disease. Therefore, the study of GC-mediated stress responses to chronic moderately stressful situations, which occur in daily life, is of huge interest for the design of pharmacological strategies toward the prevention of neurodegeneration. To address this issue, SAMP8 mice were exposed to the chronic mild stress (CMS) paradigm for 4 weeks and treated with RL-118, an 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) inhibitor. The inhibition of this enzyme is linked with a reduction in GC levels and cognitive improvement, while CMS exposure has been associated with reduced cognitive performance. The aim of this project was to assess whether RL-118 treatment could reverse the deleterious effects of CMS on cognition and behavioral abilities and to evaluate the molecular mechanisms that compromise healthy aging in SAMP8 mice. First, we confirmed the target engagement between RL-118 and 11β-HSD1. Additionally, we showed that DNA methylation, hydroxymethylation, and histone phosphorylation were decreased by CMS induction, and increased by RL-118 treatment. In addition, CMS exposure caused the accumulation of reactive oxygen species (ROS)-induced damage and increased pro-oxidant enzymes—as well as pro-inflammatory mediators—through the NF-κB pathway and astrogliosis markers, such as GFAP. Of note, these modifications were reversed by 11β-HSD1 inhibition. Remarkably, although CMS altered mTORC1 signaling, autophagy was increased in the SAMP8 RL-118-treated mice. We also showed an increase in amyloidogenic processes and a decrease in synaptic plasticity and neuronal remodeling markers in mice under CMS, which were consequently modified by RL-118 treatment. In conclusion, 11β-HSD1 inhibition through RL-118 ameliorated the detrimental effects induced by CMS, including epigenetic and cognitive disturbances, indicating that GC-excess attenuation shows potential as a therapeutic strategy for age-related cognitive decline and AD.

scholarly journals Senescent Accelerated Prone 8 (SAMP8) Mice as A Model of Age Dependent Neuroinflammation

2020 ◽  
Author(s):  
Andrés Fernández ◽  
Elena Quintana ◽  
Patricia Velasco ◽  
Belén de Andrés ◽  
Maria Luisa Gaspar ◽  
...  
Keyword(s):  
Choroid Plexus ◽  
Inflammatory Cytokines ◽  
Hippocampal Formation ◽  
Morphological Changes ◽  
Interleukin 1 ◽  
Brain Parenchyma ◽  
Age Related ◽  
Inflammatory Changes ◽  
Samp8 Mice ◽  
The Brain

Abstract Background: Aging and age related diseases are strong risk factors for the development of neurodegenerative diseases. Neuroinflammation (NIF), as the brain's immune response, plays an important role in aged associated degeneration of central nervous system (CNS). The need of animal models that will allow us to understand and modulate this process is required for the scientific community. Methods: We have analyzed aging-phenotypical and inflammatory changes of brain myeloid cells (bMyC) in a senescent accelerated prone aged (SAMP8) mouse model, and compared with their resistant to senescence control (SAMR1). We have performed morphometric methods to evaluate the architecture of cellular prolongations and analyzed Iba1+ clustered cells with aging. To analyse specific constant brain areas we have performed stereology measurements of Iba1+ cells in the hippocampal formation. We have isolated bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch), and analyzed their response to systemic LPS- driven inflammation.Results: Aged 10 month old SAMP8 mice presents many of the hallmarks of aging-dependent neuroinflammation when compared with their senescence resistant control (SAMR1); ie, increase of protein aggregates, presence of Iba1+ clusters, but not increase in the number of Iba1+ cells. We have further observed and increased of main inflammatory mediator IL-1β, and augment of border MHCII+Iba1+ cells. Isolated CD45+ bMyC from brain parenchyma (BP) and choroid plexus and meningeal membranes (m/Ch) have been analyzed showing that there is not significant increase of CD45+ from the periphery. Our data support that aged-driven pro-inflammatory cytokine interleukin 1 beta (IL1β) transcription is mainly enhanced in CD45+BP cells. Furthermore, we are showing that LPS-driven systemic inflammation produces inflammatory cytokines mainly in the border bMyC, sensed to a lesser extent by the BP bMyC, and is enhanced in aged SAMP8 compared to control SAMR1.Conclusion: Our data validate the SAMP8 model to study age-associated neuroinflammatory events, but careful controls for age and strain are required. These animals show morphological changes in their bMyC cell repertoires associated to age, corresponding to an increase in the production of main pro inflammatory cytokines such as IL-1β, which predispose the brain to an enhanced inflammatory response after LPS-systemic challenge.

The Antioxidant Resveratrol from Polygonum Cuspidatum Reverses Memory Impairment and Brain Oxidative Stress in SAMP8 Mice

2011 ◽  
Vol 422 ◽  
pp. 470-473
Author(s):  
Gui Shan Liu ◽  
Ze Sheng Zhang ◽  
Bo Yang ◽  
Wei He
Keyword(s):  
Oxidative Stress ◽  
Learning And Memory ◽  
Open Field ◽  
Field Test ◽  
Memory Impairment ◽  
Open Field Test ◽  
Pharmacological Action ◽  
Age Related ◽  
Brain Oxidative Stress ◽  
Samp8 Mice

Resveratrol (RVT) is a phytoalexin polyphenolic compound found in various plants, including grapes, berries and peanuts. Recently, studies have documented various health benefits of resveratrol including cardiovascular and cancer-chemopreventive properties. The aim of the present study was to demonstrate the effects of resveratrol on the learning and memory impairment. The senescence-accelerated mice (SAM) were introgastric gavage administrated resveratrol (25,100mg/(kg•bw)) for 60 days. The learning and memory behavior was assessed using open-field test while the parameters of oxidative stress assessed were malondialdehyde (MDA) and superoxide dismutases (SOD).The results showed that resveratrol significantly improved the learning and memory ability in open-field test. Further investigation showed that resveratrol restored SOD levels, but decreased MDA level in the mouce brain. These results indicated that the pharmacological action of RVT may offer a novel therapeutic strategy for the treatment of age-related conditions.

Effects of moderate exercise over different phases on age-related physiological dysfunction in testes of SAMP8 mice

2013 ◽  
Vol 48 (9) ◽  
pp. 869-880 ◽  
Author(s):  
Xiujun Zhao ◽  
Yanqing Bian ◽  
Yichong Sun ◽  
Li Li ◽  
Lixuan Wang ◽  
...  
Keyword(s):  
Moderate Exercise ◽  
Age Related ◽  
Samp8 Mice

scholarly journals INCREASED C3 IN THE AGING BRAIN PROMOTES INFLAMMATORY TRANSITION IN ENDOTHELIAL CELLS

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S840-S840
Author(s):  
Nicholas E Propson ◽  
Alexandra Litvinchuk ◽  
Ethan R Roy ◽  
Bianca Contreras ◽  
Wei Cao ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Disease Onset ◽  
Strong Relationship ◽  
Complement C3 ◽  
Aging Brain ◽  
Aged Mouse ◽  
Dependent Manner ◽  
Brain Vasculature ◽  
Age Related ◽  
Bbb Permeability

Abstract Innate immunity has been implicated in normal aging, and age-related disease. The connection between age-related neuroinflammation and change in brain vasculature prior to disease onset remains poorly understood. The complement pathway is an established mediator of neuroinflammation, and increased complement C3 is seen in the aging brain. Thus, we asked whether C3 can promote changes in brain vasculature. We found age dependent increase of brain C3 levels in C57BL/6J mice. Furthermore, we found an increase in expression of adhesion molecule VCAM-1 in endothelial cells (ECs) of the cortex and hippocampus, which was rescued in aged C3a receptor null (C3ar1-/-) mice and aged C3a receptor (C3aR) antagonist treated mice. We confirmed these results by qPCR analysis for Vcam1 in sorted ECs. Human brain microvascular endothelial cells (HBMECs) treated with C3a showed increased expression of VCAM-1, but not other adhesion molecules. Sorted ECs from C3ar1-/- mice challenged with LPS confirmed these findings. Furthermore, C3aR signaling in ECs showed increased blood-brain barrier (BBB) permeability using trans-endothelial electrical resistance (TEER), and BBB impermeable dye injections. HBMECs treated with C3a revealed mis-localization of VE-Cadherin, followed by reduction in protein level when analyzed by immunofluorescence, which promotes increased barrier permeability. As a functional consequence of VCAM-1 expression and increased BBB permeability we found aged mouse brains have increased peripheral lymphocyte (CD45+/CD11b-) infiltration, which was reduced in a C3aR dependent manner. In conclusion, our work suggests there is a strong relationship between C3 expression and vascular C3aR contributing to a functional transition in endothelial cells during aging.

scholarly journals Long-Term Feeding of a High-Fat Diet Ameliorated Age-Related Phenotypes in SAMP8 Mice

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1416
Author(s):  
Hideaki Oike ◽  
Yukino Ogawa ◽  
Kayo Azami
Keyword(s):  
Control Diet ◽  
Active Phase ◽  
Restricted Feeding ◽  
Long Term Effects ◽  
High Fat ◽  
Night Time ◽  
Age Related ◽  
Nutritional Studies ◽  
Samp8 Mice

High-fat diets (HFD) have been thought to increase the risk of obesity and metabolic syndrome, as well as shorten lifespan. On the other hand, chrono-nutritional studies have shown that time-restricted feeding during active phase significantly suppresses the induction of HFD-induced obesity in mouse model. However, the long-term effects of time-restricted HFD feeding on aging are unknown. Therefore, in this study, we set up a total of four groups: mutual combination of ad libitum feeding or night-time-restricted feeding (NtRF) and an HFD or a control diet. We examined their long-term effects in a senescence-accelerated mouse strain, SAMP8, for over a year. Hearing ability, cognitive function, and other behavioral and physiological indexes were evaluated during the study. Unexpectedly, SAMP8 mice did not show early onset of death caused by the prolonged HFD intake, and both HFD and NtRF retarded age-related hearing loss (AHL). NtRF improved grip strength and cognitive memory scores, while HFD weakly suppressed age-related worsening of the appearance scores associated with the eyes. Notably, the HFD also retarded the progression of AHL in both DBA/2J and C57BL/6J mice. These results suggest that HFD prevents aging unless metabolic disorders occur and that HFD and NtRF are independently effective in retarding aging; thus, the combination of HFD and chrono-nutritional feeding may be an effective anti-aging strategy.

Sign in / Sign up

Export Citation Format

Share Document