Aerobic exercise repairs neurological function after cerebral ischaemia by regulating the nitric oxide

Sun, Lirong; Zhuang, Lv-Ping; Wang, Weifeng

doi:10.1590/0001-3765201920190068

Cited by 3 publications

(4 citation statements)

References 24 publications

(11 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Different modalities of swimming exercise are known to elicit a preconditioning effect [ 73 , 74 ], able to attenuate or reverse cerebral injury in the early stage after ischemia [ 75 ], and improve cognition [ 76 ]. Furthermore, NO production from the three NOS isoforms [ 77 ] and increased hydroxyl radical rate [ 78 ] triggered by aerobic exercise participate in the formation of associative and spatial memory [ 79 ]. Our results in the temporoparietal cortex in the MWM group showed that swimming exercise during the late stage of ischemia increased lipid peroxidation, iNOS, and eNOS, events also associated with improved sensory and motor skills [ 80 ], spatial recognition, and long-term learning and memory [ 81 ].…”

Section: Discussionmentioning

confidence: 99%

“…In contrast, the prevention of cognitive deficits and tissue damage was achieved with the addition of subacute prophylactic zinc administration. eNOS likely mediates this beneficial effect since exercise prevents vascular endothelium dysfunction [ 77 , 84 , 85 ], reduces infarct volume [ 86 ], and promotes nerve repair after cerebral ischemia [ 77 ]. Furthermore, zinc stabilizing eNOS increases its enzymatic activity [ 87 ].…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Prophylactic Zinc Administration Combined with Swimming Exercise Prevents Cognitive-Emotional Disturbances and Tissue Injury following a Transient Hypoxic-Ischemic Insult in the Rat

Aguilar-Peralta

Gonzalez-Vazquez

Tomás-Sanchez

et al. 2022

Behavioural Neurology

View full text Add to dashboard Cite

Exercise performance and zinc administration individually yield a protective effect on various neurodegenerative models, including ischemic brain injury. Therefore, this work was aimed at evaluating the combined effect of subacute prophylactic zinc administration and swimming exercise in a transient cerebral ischemia model. The prophylactic zinc administration (2.5 mg/kg of body weight) was provided every 24 h for four days before a 30 min common carotid artery occlusion (CCAO), and 24 h after reperfusion, the rats were subjected to swimming exercise in the Morris Water Maze (MWM). Learning was evaluated daily for five days, and memory on day 12 postreperfusion; anxiety or depression-like behavior was measured by the elevated plus maze and the motor activity by open-field test. Nitrites, lipid peroxidation, and the activity of superoxide dismutase (SOD) and catalase (CAT) were assessed in the temporoparietal cortex and hippocampus. The three nitric oxide (NO) synthase isoforms, chemokines, and their receptor levels were measured by ELISA. Nissl staining evaluated hippocampus cytoarchitecture and Iba-1 immunohistochemistry activated the microglia. Swimming exercise alone could not prevent ischemic damage but, combined with prophylactic zinc administration, reversed the cognitive deficit, decreased NOS and chemokine levels, prevented tissue damage, and increased Iba-1 (+) cell number. These results suggest that the subacute prophylactic zinc administration combined with swimming exercise, but not the individual treatment, prevents the ischemic damage on day 12 postreperfusion in the transient ischemia model.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Prophylactic Zinc Administration Combined with Swimming Exercise Prevents Cognitive-Emotional Disturbances and Tissue Injury following a Transient Hypoxic-Ischemic Insult in the Rat

Aguilar-Peralta

Gonzalez-Vazquez

Tomás-Sanchez

et al. 2022

Behavioural Neurology

View full text Add to dashboard Cite

show abstract

“…Exercise reduced brain injury following cerebral ischemia and restored impaired eNOS- and nNOS-dependent vascular function in type 1 diabetic rats ( Arrick et al, 2012 ). Sun et al (2019) indicated that exercise and exhaustive exercise animals both had higher expression of NO, increased NOS activity, and elevated expression of eNOS, nNOS, and iNOS. Interestingly, levels of eNOS are much higher within the exercise group, while iNOS has a significant increase in the exhaustive exercise group, which suggests that exercise can exert a neuroprotective effect by promoting levels of eNOS but not iNOS.…”

Section: Exercise and Restoration Of Neurovascular Unitmentioning

confidence: 98%

Neuroprotective Effect of Physical Activity in Ischemic Stroke: Focus on the Neurovascular Unit

Zhang

Xie

2022

Front. Cell. Neurosci.

View full text Add to dashboard Cite

Cerebral ischemia is one of the major diseases associated with death or disability among patients. To date, there is a lack of effective treatments, with the exception of thrombolytic therapy that can be administered during the acute phase of ischemic stroke. Cerebral ischemia can cause a variety of pathological changes, including microvascular basal membrane matrix, endothelial cell activation, and astrocyte adhesion, which may affect signal transduction between the microvessels and neurons. Therefore, researchers put forward the concept of neurovascular unit, including neurons, axons, astrocytes, microvasculature (including endothelial cells, basal membrane matrix, and pericyte), and oligodendrocytes. Numerous studies have demonstrated that exercise can produce protective effects in cerebral ischemia, and that exercise may protect the integrity of the blood-brain barrier, promote neovascularization, reduce neuronal apoptosis, and eventually lead to an improvement in neurological function after cerebral ischemia. In this review, we summarized the potential mechanisms on the effect of exercise on cerebral ischemia, by mainly focusing on the neurovascular unit, with the aim of providing a novel therapeutic strategy for future treatment of cerebral ischemia.

show abstract

“…There are three types of NOS: endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS). The iNOS is the major NOS isoform in the brain (Sun et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Effects of Mongolian Warm Acupuncture on iNOS/NO and Inflammatory Cytokines in the Hippocampus of Chronic Fatigue Rats

Shui

et al. 2020

Front. Integr. Neurosci.

View full text Add to dashboard Cite

The inducible nitric oxide synthase/nitric oxide (iNOS/NO) signaling pathway and inflammatory cytokines play important roles in the pathogenesis of exercise-induced fatigue. Studies have found that Mongolian warm acupuncture (WA) could alleviate exercise-induced fatigue. However, the exact mechanisms underlying its effects remain unclear. In the present study, we investigated the effects of Mongolian WA on iNOS/NO signaling pathway and proinflammatory cytokines in a chronic exhaustive swimminginduced fatigue rat model. Animals were randomly divided into Control group, Ctrl + WA group, Model group, and Model + WA group. The body weight, exhaustive swimming time test, and Morris water maze test were performed before and after the chronic exhaustive swimming. The serum levels of interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ), and iNOS were detected by enzyme linked immunosorbent assay (ELISA). The mRNA expressions of IL-1β, IL-6, TNF-α, IFN-γ, and iNOS in the hippocampus were measured by real-time polymerase chain reaction (RT-PCR). Moreover, the protein expression of iNOS in the hippocampus was measured by western blot, and the NO productions in the serum and hippocampus were detected by Griess reaction system. Chronic exhaustive exercise significantly reduced the body weight and exhaustive swimming time, and induced impairment in learning and memory, and which were reversed by WA treatment. Chronic exhaustive exercise also increased the expressions of iNOS and proinflammatory cytokines, while WA treatment significantly decreased the level of iNOS and proinflammatory cytokines. However, chronic exhaustive exercise did not affect the NO production. These findings demonstrated that WA could alleviate the chronic exhaustive swimming-induced fatigue and improve the learning and memory ability, and the actions might be related to the reduction of inflammatory response and iNOS expression.

show abstract

Aerobic exercise repairs neurological function after cerebral ischaemia by regulating the nitric oxide

Cited by 3 publications

References 24 publications

Prophylactic Zinc Administration Combined with Swimming Exercise Prevents Cognitive-Emotional Disturbances and Tissue Injury following a Transient Hypoxic-Ischemic Insult in the Rat

Prophylactic Zinc Administration Combined with Swimming Exercise Prevents Cognitive-Emotional Disturbances and Tissue Injury following a Transient Hypoxic-Ischemic Insult in the Rat

Neuroprotective Effect of Physical Activity in Ischemic Stroke: Focus on the Neurovascular Unit

Effects of Mongolian Warm Acupuncture on iNOS/NO and Inflammatory Cytokines in the Hippocampus of Chronic Fatigue Rats

Contact Info

Product

Resources

About