scholarly journals OXIDATIVE CHANGES AND COGNITIVE FUNCTION DECLINE IN AGING RATS

Author(s):  
MUHAMMAD IRFAN NORMAN FRANCIS RUDIN ◽  
SUZANA MAKPOL ◽  
WAN ZURINAH WAN NGAH ◽  
YASMIN ANUM MOHD YUSOF

Objective: This study aims to show that impairment of cognitive function occurred during aging is related to increased oxidative stress. Methods: A total of 36 Sprague Dawley rats were divided into four groups: Young (3 months), middle (14 months), and old age groups (18 and 23 months). Rats were killed and blood was collected for the measurement of oxidative stress which includes deoxyribonucleic acid (DNA) damage and lipid peroxidation (malondialdehyde [MDA] levels). Cognitive function of rats was measured through open-field experiments, Morris water maze (MWM), and object identification. Results: Increased DNA damage and MDA levels were found in middle age and old rats compared to young rats (3 months old, p<0.05). There was an increase in anxiety with age as indicated by the increased production of fecal boli and decreased activity of grooming and rearing. For the navigation test, older rats took a long time to search for the hidden platform compared to young rats. In the probe test (spatial memory test 24 h after the last training), the middle- and old-age groups spent less time at the quadrant compared to the young age group. Conclusion: There is a decline in cognitive function with increased oxidative stress in aging rats.

2009 ◽  
Vol 111 (1) ◽  
pp. 64-71 ◽  
Author(s):  
Xinzhu Pu ◽  
Lisa M. Kamendulis ◽  
James E. Klaunig

2016 ◽  
Vol 42 (5-6) ◽  
pp. 297-309 ◽  
Author(s):  
Pia Horvat ◽  
Ruzena Kubinova ◽  
Andrzej Pajak ◽  
Abdonas Tamosiunas ◽  
Ben Schöttker ◽  
...  

Background/Aims: Oxidative stress is involved in Alzheimer disease pathology, but its impact on cognitive function in community-dwelling older adults remains unknown. We estimated associations between serum oxidative stress markers and cognitive function in early old age. Methods: Subjects aged 45-69 years recruited in urban centers in Central and Eastern Europe had memory, verbal fluency, and processing speed assessed at baseline (2002-2005) and 3 years later. Derivatives of reactive oxygen metabolites (d-ROMs), biological antioxidant potential (BAP), and total thiol levels (TTLs) were measured at baseline in a subsample. Linear regression was used to estimate associations of biomarkers with cognitive test scores cross-sectionally (n = 4,304) and prospectively (n = 2,882). Results: Increased d-ROM levels were inversely associated with global cognition and verbal fluency cross-sectionally and in prospective analysis; observed effects corresponded to 3-4 years' higher age. TTL was inconsistently associated with memory. BAP was not related to cognitive function. Conclusion: This study found modest evidence for a relationship between serum d-ROMs and cognitive function in a population sample of older adults.


2019 ◽  
Vol 47 (8) ◽  
pp. 3860-3873 ◽  
Author(s):  
Pei-Rong Liu ◽  
Feng Cao ◽  
Yu Zhang ◽  
Sheng Peng

Objectives To investigate the effects of electroacupuncture in regulating astrocytes and oxidative stress in a rat model of postoperative cognitive dysfunction (POCD). Methods Male aged Sprague-Dawley rats were randomized to undergo left hepatic lobe resection to induce POCD, followed by either electroacupuncture or no treatment; or similar surgery without left lobe resection or electroacupuncture (sham). Postsurgical cognitive function, hippocampal astrocyte number and oxidative stress indicators were measured. Results At days 1, 3 and 7 following surgery, escape latency was significantly shorter and platform crossing frequency was increased with electroacupuncture versus other groups. At postoperative day 1, the electroacupuncture group showed significantly fewer glial fibrillary acidic protein (GFAP)-positive hippocampal astrocytes versus the POCD model group. In POCD rats, electroacupuncture significantly decreased serum S100 calcium binding protein B and neuron-specific enolase levels, and increased brain-derived neurotrophic factor and glial cell-derived neurotrophic factor levels, at days 1, 3 and 7. Electroacupuncture significantly attenuated the hippocampal POCD-induced increase in malondialdehyde and decreased superoxide dismutase levels at day 1 following surgery. Conclusion Electroacupuncture may improve cognitive function in rats with POCD by reducing hippocampal GFAP-positive astrocyte number and suppressing oxidative stress.


2020 ◽  
Vol 11 (4) ◽  
pp. 7827-7832
Author(s):  
Zainie Aboo Bakkar ◽  
Nooraqilah Rubaai ◽  
Nur Afiqah Mahazi ◽  
Nurhanisah Hosni ◽  
Nik Nur Nadia Nik Mat ◽  
...  

Disused muscle atrophy (DMA) causes severe problems in aging society especially bedridden people. Oxidative stress is proposed to be involved in the pathogenesis of DMA. Hibiscus sabdariffa L.  (HS) or roselle contains high flavonoids, a compound previously shown to be an effective antioxidant, antihypertensive and antidiabetic agent. Thus, the present study investigated the protective effects of HS against oxidative stress in the hind limb of immobilized rats. Twenty-eight male Sprague-Dawley rats were randomly divided into four groups (n=6 per group): Control group received no intervention; Immobilized group received unilateral hind limb immobilization for five days; HS group received 100 mg/kg/bw through oral force feeding for 28 days; Immobilized + HS group received unilateral hind limb immobilization for five days followed by 28-days HS treatment with the same dosage. Blood samples were collected and analysed for DNA damage, lipid peroxidation and oxidative enzyme. Data were presented as mean ± SEM and statistically analysed by ANOVA. The results showed a significant increase in percentage of mild DNA damage after HS treatment in hind limb immobilized rat (Control: 86.5±1.4%; Immobilized: 25.0±5.5%; HS: 37.0±3.5%; Immobilized + HS: 56.7±7.9%, P=0.003). There was also significant increase in plasma catalase activity after HS treatment (plasma [hydrogen peroxide] in Control: 72.5±0.3 µg/ml; Immobilized: 65.1±1.3 µg/ml; HS: 68.3±3.2 µg/ml; Immobilized + HS: 56.5±4.9 µg/ml, P=0.006) but not in plasma malondialdehyde (MDA) level. In conclusion, these findings suggested that HS treatment may prevent oxidative stress-induced DMA in the rats' hind limb immobilization model.


1998 ◽  
Vol 274 (5) ◽  
pp. H1509-H1515 ◽  
Author(s):  
Norman R. Harris ◽  
Kimberly W. Langlois

The age-dependent responses of the mesenteric vasculature to ischemia-reperfusion (I/R) were compared in 2-mo-old and 2-yr-old rats. Measurements were made of leukocyte adherence, albumin leakage, and oxidative stress in postcapillary venules. In young rats I/R induced an increase in leukocyte adherence and albumin leakage, but in aged rats I/R induced an increase in albumin leakage without an increase in leukocyte adherence. Furthermore, I/R-induced oxidative stress was higher in the aged rats than in the young rats. To investigate whether the age-associated oxidative stress is related to a decrease in the role of nitric oxide, NG-nitro-l-arginine methyl ester (l-NAME) was superfused onto the mesentery of young and aged rats.l-NAME induced an increase in postcapillary protein leakage only in young rats; however, arteriolar constriction induced byl-NAME occurred in both age groups. These results suggest that different mechanisms contribute to the inflammatory responses and microvascular dysfunction elicited by I/R in young and aged rats.


2009 ◽  
Vol 24 (1) ◽  
pp. 66-73 ◽  
Author(s):  
Anita K. Patlolla ◽  
Constance Barnes ◽  
Clement Yedjou ◽  
V. R. Velma ◽  
Paul B. Tchounwou

2020 ◽  
Vol 2020 ◽  
pp. 1-10
Author(s):  
Jing Huang ◽  
Botong Hou ◽  
Shuaimei Zhang ◽  
Meiyao Wang ◽  
Xuanzhen Lu ◽  
...  

Aging is a multifactorial process involving the cumulative effects of inflammation, oxidative stress, and mitochondrial dynamics, which can produce complex structural and biochemical alterations to the nervous system and lead to dysfunction of microcirculation, blood-brain barrier (BBB), and other problems in the brain. Long-term injection of D-galactose (D-gal) can induce chronic inflammation and oxidative stress, accelerating aging. The model of accelerated aging with long-term administration of D-gal have been widely used in anti-aging studies, due to the increase of chronic inflammation and decline of cognition that similarity with natural aging in animals. However, despite extensive researches in the D-gal-induced aging rats, studies on their microvasculature remain limited. Endothelial progenitor cells (EPCs), which are precursors to endothelial cells (ECs), play a significant role in the repair and regeneration process of endogenous blood vessel, and adiponectin (APN), a protein derived from adipocyte, has many effects on protective vascular endothelium and anti-inflammatory. Recently, many studies have shown that APN can promote improvements in cognitive function. Under these circumstances, we investigated the neuroprotective effect of the APN-transfected EPC (APN-EPC) treatment on rats after administration with D-gal and explored the likely underlying mechanisms. Compared to model group for D-gal administration, better cognitive function and denser microvessels were significantly found in the APN-EPC treatment group, and indicated APN-EPC treatment in aging rats could improve the cognitive dysfunction and microvessel density. The level of proinflammatory cytokines IL-1β, IL-6, and TNF-α, activated astrocytes and apoptosis rate were significantly reduced in the APN-EPC group compared with the model group, showed that APN-EPCs alleviated the neuroinflammation in aging rats. In addition, the APN-EPC group inhibited the decrease of BBB-related proteins claudin-5, occludin, and Zo-1 in aging rats and attenuated BBB dysfunction significantly. These results of our study indicated that APN-EPC treatment in D-gal-induced aging rats have a positive effect on improving cognitive and BBB dysfunction, increasing angiogenesis, and reducing neuroinflammation and apoptosis rate. This research suggests that cell therapy via gene modification may provide a safe and effective approach for the treatment of age-related neurogenerative diseases.


2020 ◽  
Vol 21 (8) ◽  
pp. 667-680
Author(s):  
Jing-zhi Wan ◽  
Rui Wang ◽  
Zhi-yong Zhou ◽  
Li-li Deng ◽  
Chang-cheng Zhang ◽  
...  

Background: Oxidative stress and mitochondrial dysfunction play a vital role in the pathogenesis of brain aging. Saponins from Panax japonicus (SPJ) have attracted much attention for their potential to attenuate age-related oxidative stress as the main ingredient in rhizomes of Panax japonicus. Objective: This study aimed to investigate the neuroprotective effects of SPJ on natural aging rats as well as the underlying mechanisms regarding oxidative stress and mitochondrial pathway. Methods: Sprague-Dawley rats were divided into control groups (3-, 9-, 15- and 24-month old groups) and SPJ-treated groups. For SPJ-treated groups, SPJ were orally administrated to 18-month old rats at doses of 10 mg/kg, 30 mg/kg and 60 mg/kg once daily. Control groups were given the same volume of saline. After the treatment with SPJ or saline for six months, the cortex and hippocampus were rapidly harvested and deposited at -80°C after the rats were decapitated under anesthesia. The neuroprotective effects of SPJ were estimated by histopathological observation, TUNEL detection, biochemical determination and western blotting. Results: SPJ improved pathomorphological changes in neuronal cells and decreased apoptosis in the cortex and hippocampus of aging rats, increased the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), Na+/K+-ATPase, Ca2+-ATPase and Ca2+/Mg2+-ATPase whereas, decreased malondialdehyde (MDA) contents in the cortex of aging rats. Furthermore, the SPJ increased silent mating type information regulation 2 homolog-1 (SIRT1) protein expression, decreased acetylated level of peroxisome proliferator-activated receptor-γ coactivator-1α (PGC-1α) in the cortex and hippocampus of aging rats, and reversed the aging-induced decline of Forkhead box O3 (Foxo3a), Superoxide Dismutase 2 (SOD2), microtubule-associated protein light chain 3 (LC3II) and Beclin1 levels in the cortex and hippocampus. Conclusion: Our data showed that SPJ conferred neuroprotection partly through the regulation of oxidative stress and mitochondria-related pathways in aging rats.


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