scholarly journals 3,4-Dihydroxybenzalacetone (DBL) Prevents Aging-Induced Myocardial Changes in Senescence-Accelerated Mouse-Prone 8 (SAMP8) Mice

Cells ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 597
Author(s):  
Vijayasree V. Giridharan ◽  
Vengadeshprabhu Karupppagounder ◽  
Somasundaram Arumugam ◽  
Yutaka Nakamura ◽  
Ashrith Guha ◽  
...  
Keyword(s):  
Dna Damage ◽  
Oxidative Dna Damage ◽  
Cardiac Fibrosis ◽  
Myocardial Dysfunction ◽  
The Elderly ◽  
Tunel Staining ◽  
Inonotus Obliquus ◽  
Age Related ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse

Aging is a predominant risk factor for the development and progression of cardiovascular complications. Physiologically and anatomically, the heart undergoes numerous changes that result in poor cardiac function in the elderly population. Recently, several studies have provided promising results, confirming the ability of the senescence-accelerated mouse-prone 8 (SAMP8) model to accurately model age-related cardiovascular alterations. In this study, using a murine model of senescence, SAMP8, we aimed to investigate the effect of 3,4-dihydroxybenzalacetone (DBL), a catechol-containing phenylpropanoid derivative isolated from Inonotus obliquus (Chaga), on cardiac aging. DBL was administered at the doses of 10 mg/kg and 20 mg/kg by oral gavage to SAMP8 mice to examine aging-mediated cardiac changes, such as oxidative DNA damage, oxygen radical antioxidant capacity (ORAC) value, fibrosis, inflammation, and apoptosis. The treatment with DBL at both doses significantly reduced aging-mediated oxidative DNA damage, and simultaneously increased the ORAC value in the SAMP8 assay. Cardiac fibrosis was assessed with Azan-Mallory staining, and the number of cardiac remodeling markers was found to be significantly reduced after the treatment with DBL. We also observed a decrease in cardiomyocyte apoptosis as measured by the terminal transferase-mediated dUTP nick end labeling (TUNEL) staining method and the caspase-3 levels in SAMP8 mice compared with senescence-resistant control (SAMR1) mice. The findings from this study suggest that DBL has a potentially beneficial effect on aging-mediated myocardial alterations. Further studies are warranted to confirm the promising potential of this catechol compound against aging-associated myocardial dysfunction.

Degenerative cardiovascular disease in the elderly

ESC CardioMed ◽  
2018 ◽  
pp. 2960-2964
Author(s):  
Edgar Argulian
Keyword(s):  
Aortic Valve ◽  
Cardiac Fibrosis ◽  
Prognostic Significance ◽  
The Elderly ◽  
Degenerative Changes ◽  
Ageing Population ◽  
Mitral Annular Calcification ◽  
Aortic Valve Sclerosis ◽  
Age Related ◽  
Annular Calcification

The ageing population represents a unique challenge for cardiovascular care. Ageing causes remodelling of the cardiovascular system and commonly results in distinct degenerative changes. Most of these degenerative changes have significant interactions with cardiovascular risk factors by either being a marker of disease burden or being exaggerated by co-morbid conditions. Also, age-related degenerative conditions have physiological and prognostic implications. This chapter discusses several common degenerative cardiovascular conditions in the elderly such as cardiac fibrosis, amyloidosis, mitral annular calcification, and aortic valve sclerosis. Some of these conditions (such as cardiac fibrosis and amyloidosis) are implicated in pathogenesis of heart failure with preserved ejection fraction. Others (such as mitral annular calcification and aortic valve sclerosis) do not typically cause any measurable physiological abnormality but have prognostic significance.

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.

Age-Related Sex Differences in Glutathione Peroxidase and Oxidative DNA Damage in a Healthy Mexican Population

2010 ◽  
Vol 19 (5) ◽  
pp. 919-926 ◽  
Author(s):  
Víctor Manuel Mendoza-Núñez ◽  
Ada Beristain-Pérez ◽  
Silvia Patricia Pérez-Vera ◽  
Mario A. Altamirano-Lozano
Keyword(s):  
Dna Damage ◽  
Sex Differences ◽  
Glutathione Peroxidase ◽  
Oxidative Dna Damage ◽  
Mexican Population ◽  
Age Related

Age-related changes in the oestrous cycle and reproductive hormones in senescence-accelerated mouse

2005 ◽  
Vol 17 (5) ◽  
pp. 507 ◽  
Author(s):  
Ma Yuan ◽  
Zhou Wen-Xia ◽  
Cheng Jun-Ping ◽  
Zhang Yong-Xiang
Keyword(s):  
Substance P ◽  
Luteinising Hormone ◽  
Reproductive Hormones ◽  
Oestrous Cycle ◽  
Reproductive Hormone ◽  
Hormone Levels ◽  
Age Related ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse ◽  
Age Related Changes

To investigate age-related changes in the oestrous cycle and reproductive hormone levels in senescence-accelerated mouse (SAM), we examined these parameters in 3-, 5-, 7-, 9- and 11-month-old female SAM-prone/8 (SAMP8) and SAM-resistant/1 (SAMR1) strains. Levels of β-endorphin (β-EP) and substance P (SP) in the hypothalamus were also measured. The oestrous cycle and dioestrus of 9-month-old SAMP8 mice were significantly prolonged compared with age-matched SAMR1 mice. Furthermore, the concentration of serum oestradiol was lower and the level of pituitary luteinising hormone was higher in SAMP8 mice compared with SAMR1 mice. This characterises the hypothalamus–pituitary–ovary (HPO) axis of the SAMP8 strain as hypergonadotropic–hypogonad. The levels of β-EP and SP in the SAMP8 hypothalamus were lower than in the SAMR1 hypothalamus. These results indicate that the function of the HPO axis in SAMP8 mice declines early and this may be attributed, in part, to the decline in β-EP and SP concentrations in the hypothalamus.

Erratum to: Age-related changes in the oestrous cycle and reproductive hormones in senescence-accelerated mouse

2009 ◽  
Vol 21 (4) ◽  
pp. 624
Author(s):  
Ma Yuan ◽  
Zhou Wen-Xia ◽  
Cheng Jun-Ping ◽  
Zhang Yong-Xiang
Keyword(s):  
Substance P ◽  
Luteinising Hormone ◽  
Reproductive Hormones ◽  
Oestrous Cycle ◽  
Reproductive Hormone ◽  
Hormone Levels ◽  
Age Related ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse ◽  
Age Related Changes

To investigate age-related changes in the oestrous cycle and reproductive hormone levels in senescence-accelerated mouse (SAM), we examined these parameters in 3-, 5-, 7-, 9- and 11-month-old female SAM-prone/8 (SAMP8) and SAM-resistant/1 (SAMR1) strains. Levels of �-endorphin (�-EP) and substance P (SP) in the hypothalamus were also measured. The oestrous cycle and dioestrus of 9-month-old SAMP8 mice were significantly prolonged compared with age-matched SAMR1 mice. Furthermore, the concentration of serum oestradiol was lower and the level of pituitary luteinising hormone was higher in SAMP8 mice compared with SAMR1 mice. This characterises the hypothalamus.pituitary.ovary (HPO) axis of the SAMP8 strain as hypergonadotropic.hypogonad. The levels of �-EP and SP in the SAMP8 hypothalamus were lower than in the SAMR1 hypothalamus. These results indicate that the function of the HPO axis in SAMP8 mice declines early and this may be attributed, in part, to the decline in �-EP and SP concentrations in the hypothalamus.

Age-related autophagy alterations in the brain of senescence accelerated mouse prone 8 (SAMP8) mice

2011 ◽  
Vol 46 (7) ◽  
pp. 533-541 ◽  
Author(s):  
Qinying Ma ◽  
Jing Qiang ◽  
Ping Gu ◽  
Yanyong Wang ◽  
Yuan Geng ◽  
...  
Keyword(s):  
Age Related ◽  
Samp8 Mice ◽  
The Brain ◽  
Senescence Accelerated Mouse

Modulatory role of grape seed extract on age-related oxidative DNA damage in central nervous system of rats

2006 ◽  
Vol 68 (6) ◽  
pp. 469-473 ◽  
Author(s):  
Muthaiya Balu ◽  
Purushotham Sangeetha ◽  
Ganesan Murali ◽  
Chinnakannu Panneerselvam
Keyword(s):  
Central Nervous System ◽  
Dna Damage ◽  
Nervous System ◽  
Oxidative Dna Damage ◽  
Grape Seed Extract ◽  
Grape Seed ◽  
Seed Extract ◽  
Age Related

scholarly journals The different functions of exercise, supplementary resveratrol, and the combination of exercise and supplementary resveratrol in young and old SAMP8 mice liver

2020 ◽  
Author(s):  
Sergey Suchkov ◽  
Jia-Ping Wu
Keyword(s):  
Cytochrome C ◽  
Western Blot ◽  
Cross Sections ◽  
Tunel Staining ◽  
Mice Liver ◽  
Related Liver Disease ◽  
Samp8 Mice ◽  
Senescence Accelerated Mouse ◽  
Hematoxylin Eosin ◽  
Better Than

AbstractThe senescence-accelerated mouse prone 8 (SAMP8) has about half the normal lifespan of a rodent. Therefore, we determined whether the different age degrees has rapid physiological senescence with the same interaction function and mechanism of exercise and supplementary resveratrol intake by SAMP8 mice liver. Histological of aging related liver disease was examined SAMP8 mice by hematoxylin-eosin and Masson’s trichrome staining.Apoptosis was determined by TUNEL staining. The mechanism proteins expression of p-PI3K/PI3K, p-Akt/Akt, Bad, cytochrome c, Bcl 2, ERK1, IL-6, STAT3, MEK5, p-ERK5/ERK5, FGF2, and MMP2/9 were examined by western blot. Results showed that the 3- and 6-month-old SAMP8 mice liver, the senescence-accelerated liver cross-sections observed adipocytes, collagen, and apoptosis cells appear, but lower occurs by exercise, supplementary resveratrol, and their combination. Combination exercise and supplementary resveratrol at the 6-month-old SAMP8 mice has significant increase ratio by p-PI3K/PI3K compared to 3-month-old SAMP8 mice liver (p<0.01), and compared with without treatment SAMP8 mice liver. Exercise, supplementary resveratrol intake, and combined of exercise and resveratrol has facilitated p-Akt/Akt ratio increases, and ERK1/Bcl2 increases, but Bad/Cytochrome c decreases at the 6-month-old SAMP8 by western blot. IL-6/STAT3/MEK5 and p-ERK5/ERK5 ratio have good functions at 6-month-old SAMP8 mice better than 3-month-old SAMP8. FGF2/MMP2 decreases and MMP9 increases observed at the 3-month-old SAMP8 by exercise, supplementary resveratrol, and combination. Indeed, we suggest supplementary resveratrol can help exercise therapy ageing related liver diseases.

Abstract 2: Ogg1 Plays A Protective Role In Diet Induced Atherosclerosis in LDLR KO mice.

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Gantsetseg Tumurkhuu ◽  
Kenichi Shimada ◽  
Timothy R Crother ◽  
Wenxuan Zhang ◽  
Roberta Gottlieb ◽  
...  
Keyword(s):  
Dna Damage ◽  
Nlrp3 Inflammasome ◽  
Oxidative Dna Damage ◽  
Dna Damage Repair ◽  
Atherosclerotic Lesion ◽  
Tunel Staining ◽  
Aortic Tissue ◽  
Mtdna Damage ◽  
Caspase 1 ◽  
Damage Repair

Introduction: In human atherosclerosis, mitochondrial DNA (mtDNA) damage occurs in both circulating cells and the vessel wall, suggesting the importance of DNA damage repair enzymes. Mitochondria are a central regulator of NLRP3 function, which is a sensor of specific pathogen, host, and environmental danger molecules. Oxidized mtDNA can bind to and activate the NLRP3 inflammasome, which cleaves and activates interleukin-1β (IL-1β) and IL-18, cytokines that are pro-atherogenic. Ogg1, an oxoguanine glycosylase, can repair oxidized DNA. Objective: To assess the importance of the oxidative DNA damage repair gene, Ogg1, in atherogenesis. Methods and Results: To investigate the role of Ogg1 in atherogenesis, we generated Ogg1-/-Ldlr-/- mice. These mice had significantly larger plaques and greater lipid content in the aorta and the aortic root. Elevated levels of 8-OH-dG (a marker of oxidative DNA damage), Caspase-1 activation by FLICA staining, and apoptosis by TUNEL staining, were increased in Ogg1-/-Ldlr-/- animals compared with Ldlr-/- controls. Despite similar concentrations of plasma cholesterol, triglyceride, lipoprotein profile, glucose, insulin resistance, and body weight gain after 16 weeks high fat diet, serum MCP-1 was higher in Ogg1-/-Ldlr-/- mice compared with Ldlr-/- mice. Transplantation with Ogg1-/- bone marrow (BM) into irradiated recipient Ldlr-/- mice also resulted in an increase in atherosclerotic lesion size, 8-OH-dG accumulation, and IL-1β production in aortic tissue compared with control chimeric mice. However, Ogg1-/-/Nlrp3-/- BM transplanted into Ldlr-/- mice did not lead to acceleration of atherogenesis, suggesting that Ogg1 deficiency-induced acceleration of atherosclerosis was mediated by the NLRP3 inflammasome. Indeed, analysis of Ogg1-/- macrophages found a significant increase in caspase-1 activation and IL-1β secretion in these cells. Thus Ogg1 activity is anti-atherogenic. Conclusions: Our study provides direct evidence of a link between mtDNA damage, DNA damage repair enzyme OGG1, and atherosclerosis through increased inflammation via the NLRP3 inflammasome. These new data suggest that therapeutics designed to limit mtDNA damage may provide protection from atherosclerotic lesion development.

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