scholarly journals The Cyclic Feeding Regime Induces Decaying Age-Dependent Oxidative Stress and Regulates the Cell Chain of the Immunity

2016 ◽  
Vol 05 (06) ◽  
pp. 151-165
Author(s):  
Anatoly I. Bozhkov ◽  
Yuriy V. Nikitchenko ◽  
Katerina N. Lebed’ ◽  
Olena S. Linkevych ◽  
Natalia I. Kurguzova ◽  
...  
Placenta ◽  
2017 ◽  
Vol 57 ◽  
pp. 282-283
Author(s):  
Tereza Cindrova-Davies ◽  
Carolyn P. Jones ◽  
Norah ME. Fogarty ◽  
John Kingdom ◽  
Graham J. Burton

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Johanna Heid ◽  
Chiara Cencioni ◽  
Roberto Ripa ◽  
Mario Baumgart ◽  
Sandra Atlante ◽  
...  

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e8121 ◽  
Author(s):  
Mingxuan Wang ◽  
Yajuan Zheng

Glaucoma is an age-dependent disease closely related to oxidative stress and is regarded as the second leading cause of irreversible blindness worldwide. In recent years, many studies have shown that morphological and functional abnormalities of the trabecular meshwork (TM) are closely related to glaucoma, especially with respect to oxidative stress. In this review, the mechanisms of oxidative stress in the TM and treatment strategies for this condition, including strategies involving antioxidants, noncoding RNAs and exogenous compounds, are discussed. Although many questions remain to be answered, the reviewed findings provide insights for further research on oxidative stress alleviation in glaucoma and suggest new targets for glaucoma prevention.


2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Zhou Wu ◽  
Janchun Yu ◽  
Aiqin Zhu ◽  
Hiroshi Nakanishi

As the life expectancy continues to increase, the cognitive decline associated with Alzheimer’s disease (AD) becomes a big major issue in the world. After cellular activation upon systemic inflammation, microglia, the resident immune cells in the brain, start to release proinflammatory mediators to trigger neuroinflammation. We have found that chronic systemic inflammatory challenges induce differential age-dependent microglial responses, which are in line with the impairment of learning and memory, even in middle-aged animals. We thus raise the concept of “microglia aging.” This concept is based on the fact that microglia are the key contributor to the acceleration of cognitive decline, which is the major sign of brain aging. On the other hand, inflammation induces oxidative stress and DNA damage, which leads to the overproduction of reactive oxygen species by the numerous types of cells, including macrophages and microglia. Oxidative stress-damaged cells successively produce larger amounts of inflammatory mediators to promote microglia aging. Nutrients are necessary for maintaining general health, including the health of brain. The intake of antioxidant nutrients reduces both systemic inflammation and neuroinflammation and thus reduces cognitive decline during aging. We herein review our microglia aging concept and discuss systemic inflammation and microglia aging. We propose that a nutritional approach to controlling microglia aging will open a new window for healthy brain aging.


2015 ◽  
Vol 16 (12) ◽  
pp. 13989-14006 ◽  
Author(s):  
Julietta Moustaka ◽  
Georgia Tanou ◽  
Ioannis-Dimosthenis Adamakis ◽  
Eleftherios Eleftheriou ◽  
Michael Moustakas

2008 ◽  
Vol 105 (6) ◽  
pp. 1695-1705 ◽  
Author(s):  
Parco M. Siu ◽  
Emidio E. Pistilli ◽  
Stephen E. Alway

Oxidative stress increases during unloading in muscle from young adult rats. The present study examined the markers of oxidative stress and antioxidant enzyme gene and protein expressions in medial gastrocnemius muscles of aged and young adult (30 and 6 mo of age) Fischer 344 × Brown Norway rats after 14 days of hindlimb suspension. Medial gastrocnemius muscle weight was decreased by ∼30% in young adult and aged rats following suspension. When muscle weight was normalized to animal body weight, it was reduced by 12% and 22% in young adult and aged rats, respectively, after suspension. Comparisons between young adult and aged control animals demonstrated a 25% and 51% decline in muscle mass when expressed as absolute muscle weight and muscle weight normalized to the animal body weight, respectively. H2O2 content was elevated by 43% while Mn superoxide dismutase (MnSOD) protein content was reduced by 28% in suspended muscles compared with control muscles exclusively in the aged animals. Suspended muscles had greater content of malondialdehyde (MDA)/4-hydroxyalkenals (4-HAE) (29% and 58% increase in young adult and aged rats, respectively), nitrotyrosine (76% and 65% increase in young adult and aged rats, respectively), and catalase activity (69% and 43% increase in young adult and aged rats, respectively) relative to control muscles. Changes in oxidative stress markers MDA/4-HAE, H2O2, and MnSOD protein contents in response to hindlimb unloading occurred in an age-dependent manner. These findings are consistent with the hypotheses that oxidative stress has a role in mediating disuse-induced and sarcopenia-associated muscle losses. Our data suggest that aging may predispose skeletal muscle to increased levels of oxidative stress both at rest and during unloading.


1998 ◽  
Vol 854 (1 TOWARDS PROLO) ◽  
pp. 500-500
Author(s):  
SE IN OH ◽  
MEE SOOK LEE ◽  
CHANG-MO KANG ◽  
YOUNG DO KOH ◽  
KYU HWAN KIM ◽  
...  

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