Effect of early exercise on inflammatory parameters and apoptosis in CA1 area of the hippocampus following cerebral ischemia-reperfusion in rats

Dehqanizadeh, Behzad; Mohammadi, Ziya Fallah; Kalani, Abdol Hossein Taheri; Mirghani, Seyed Javad

doi:10.1016/j.brainresbull.2022.02.011

Cited by 5 publications

(3 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The results also showed that apoptotic cells in the CA1 area increased after LPS injection. This phenomenon is also consistent with many previous studies [ 30 , 36 , 53 , 54 ].…”

Section: Discussionsupporting

confidence: 94%

Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation

Zhang

Xing

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Sepsis-associated encephalopathy (SAE) is linked to increased morbidity and mortality rates in patients with sepsis. Increased cytokine production and neuronal apoptosis are implicated in the pathogenesis of the SAE. Neuroinflammation plays a major role in sepsis-induced brain injury. Thioredoxin-interacting protein (TXNIP), an inhibitor of thioredoxin, is associated with oxidative stress and inflammation. However, whether the TXNIP is involved in the sepsis-induced brain injury and the underlying mechanism is yet to be elucidated. Therefore, the present study was aimed at elucidating the effects of TXNIP knockdown on sepsis-induced brain injury and cognitive decline in mice. Lipopolysaccharide (LPS) was injected intraperitoneally to induce sepsis brain injury in mice. The virus-carrying control or TXNIP shRNA was injected into the lateral ventricle of the brain 4 weeks before the LPS treatment. The histological changes in the hippocampal tissues, encephaledema, and cognitive function were detected, respectively. Also, the 7-day survival rate was recorded. Furthermore, the alterations in microglial activity, oxidative response, proinflammatory factors, apoptosis, protein levels (TXNIP and NLRP3 inflammasome), and apoptosis were examined in the hippocampal tissues. The results demonstrated that the TXNIP and NLRP3 inflammasome expression levels were increased at 6, 12, and 24 h post-LPS injection. TXNIP knockdown dramatically ameliorated the 7-day survival rate, cognitive decline, brain damage, neuronal apoptosis, and the brain water content, inhibited the activation of microglia, downregulated the NLRP3/caspase-1 signaling pathway, and reduced the oxidative stress and the neuroinflammatory cytokine levels at 24 h post-LPS injection. These results suggested a crucial effect of TXNIP knockdown on the mechanism of brain injury and cognitive decline in sepsis mice via suppressing oxidative stress and neuroinflammation. Thus, TXNIP might be a potential therapeutic target for SAE patients.

show abstract

“…The results also showed that apoptotic cells in the CA1 area increased after LPS injection. This phenomenon is also consistent with many previous studies [ 30 , 36 , 53 , 54 ].…”

Section: Discussionsupporting

confidence: 94%

Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation

Zhang

Xing

Liu

et al. 2022

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

show abstract

“…Transient forebrain ischemia causes neuronal damage through various mechanisms, and the most reliable cell death mechanisms are oxidative stress and inflammation in the CA1 region. Ischemia activates astrocytes and www.nature.com/scientificreports/ microglia, which release large amounts of pro-inflammatory cytokines, such as IL-1β, IL-6, and TNF-α 3,5 , and produce ROS by nicotinamide adenine dinucleotide phosphate oxidase 4 . In this study, we visualized astrocytes and microglia in the hippocampal CA1 region 4 days after ischemia induction.…”

Section: Discussionmentioning

confidence: 99%

“…Interruption of blood supply to the brain in ischemic strokes causes massive neuronal loss in the brain, including the hippocampus, resulting in severe complications and reduced quality of life 2 . Various cell death mechanisms have been proposed, including oxidative stress induced by reactive oxygen species (ROS) and neuroinflammation induced by pro-inflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α) [3][4][5] . However, few therapeutics are available, except for tissue plasminogen activator, because of their low bioavailability and permeability to the blood-brain barrier.…”

mentioning

confidence: 99%

CHIP ameliorates neuronal damage in H2O2-induced oxidative stress in HT22 cells and gerbil ischemia

Hahn

Kwon

Yoon

et al. 2022

Sci Rep

View full text Add to dashboard Cite

Carboxyl terminus of Hsc70-interacting protein (CHIP) is highly conserved and is linked to the connection between molecular chaperones and proteasomes to degrade chaperone-bound proteins. In this study, we synthesized the transactivator of transcription (Tat)-CHIP fusion protein for effective delivery into the brain and examined the effects of CHIP against oxidative stress in HT22 cells induced by hydrogen peroxide (H2O2) treatment and ischemic damage in gerbils by 5 min of occlusion of both common carotid arteries, to elucidate the possibility of using Tat-CHIP as a therapeutic agent against ischemic damage. Tat-CHIP was effectively delivered to HT22 hippocampal cells in a concentration- and time-dependent manner, and protein degradation was confirmed in HT22 cells. In addition, Tat-CHIP significantly ameliorated the oxidative damage induced by 200 μM H2O2 and decreased DNA fragmentation and reactive oxygen species formation. In addition, Tat-CHIP showed neuroprotective effects against ischemic damage in a dose-dependent manner and significant ameliorative effects against ischemia-induced glial activation, oxidative stress (hydroperoxide and malondialdehyde), pro-inflammatory cytokines (interleukin-1β, interleukin-6, and tumor necrosis factor-α) release, and glutathione and its redox enzymes (glutathione peroxidase and glutathione reductase) in the hippocampus. These results suggest that Tat-CHIP could be a therapeutic agent that can protect neurons from ischemic damage.

show abstract

Exercise preconditioning mitigates brain injury after cerebral ischemia‐reperfusion injury in rats by restraining TIMP1

Meng,

Yang,

Chen

et al. 2024

Immunity Inflam & Disease

View full text Add to dashboard Cite

BackgroundCerebral ischemic disease is a common cerebrovascular disease, especially ischemic stroke. Exercise has protective functions on brain tissues following cerebral ischemia‐reperfusion injury (CIRI), but its preventive effects and mechanisms in CIRI remain unclear. We aimed to investigate the effects and mechanisms of exercise preconditioning on CIRI.MethodsThe middle cerebral artery occlusion (MCAO) operation was prepared to establish CIRI rats. All rats were randomized into the MCAO, exercise (exercise preconditioning plus MCAO operation), vector (exercise preconditioning, MCAO operation plus intraventricular injection of empty vector), and tissue inhibitor of metalloprotease 1 overexpression (OE‐TIMP1, exercise preconditioning, MCAO operation plus intraventricular injection of OE‐TIMP1) groups.ResultsThe results indicated that exercise preconditioning suppressed approximately 66.67% of neurological deficit scores and 73.79% of TIMP1 mRNA expression in MCAO rats, which were partially offset by OE‐TIMP1. The protective effects of exercise against neuron death status and cerebral infarction size in MCAO rats were reversed by OE‐TIMP1. It also confirmed that exercise weakened apoptosis and oxidative stress damage, with notable increases of B‐cell lymphoma‐2, superoxide dismutase, and glutathione peroxidase production, and evident decreases of BCL2‐associated X, caspase 3, and malondialdehyde in MCAO rats, while these effects were partially reversed by OE‐TIMP1. Additionally, the inhibitory effects of exercise on the protein levels of TIMP1, hypoxia‐inducible factor‐alpha, vascular endothelial growth factor receptor 2, vascular endothelial growth factor, and neurogenic locus notch homolog protein 1 in MCAO rats were partially reversed by OE‐TIMP1.ConclusionAltogether, exercise preconditioning had protective effects on CIRI by restraining TIMP1, which provided new therapeutic strategies for preventing CIRI.

show abstract

Effect of early exercise on inflammatory parameters and apoptosis in CA1 area of the hippocampus following cerebral ischemia-reperfusion in rats

Cited by 5 publications

References 34 publications

Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation

Thioredoxin-Interacting Protein (TXNIP) Knockdown Protects against Sepsis-Induced Brain Injury and Cognitive Decline in Mice by Suppressing Oxidative Stress and Neuroinflammation

CHIP ameliorates neuronal damage in H2O2-induced oxidative stress in HT22 cells and gerbil ischemia

Exercise preconditioning mitigates brain injury after cerebral ischemia‐reperfusion injury in rats by restraining TIMP1

Contact Info

Product

Resources

About