Treadmill exercise enhances synaptic plasticity in the ischemic penumbra of MCAO mice by inducing the expression of Camk2a via CYFIP1 upregulation

Shen, Wei-Min; Jin, Lingqin; Zhu, Anqi; Lin, Yao; Pan, Guoyuan; Zhou, Shi‐Ping; Cheng, Jing-Yan; Zhang, Jieqiong; Tu, Fengxia; Liu, Chan; Xie, Qipeng; Chen, Xiang

doi:10.1016/j.lfs.2021.119033

Cited by 16 publications

(5 citation statements)

References 35 publications

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“…[ 28 ] The Zea Longa rating scale was used to assess neurological injury, where a higher score indicated more severe neurological injury. [ 29 ] The results revealed that NM‐NPs and SNM‐NPs significantly improved the neural behavior of MCAO/R treated rats, whereas free Edv and RCD‐NPs, at the same dosage, failed to show similar results (Figure 5B). Staining of the coronal sections with 2,3,5‐triphenyl tetrazolium chloride (TTC) showed that treatment with free Edv resulted in a mean infarct volume of 36.09 ± 5.46%, and this did not significantly differ from the control treated with Saline (38.24 ± 2.31%).…”

Section: Resultsmentioning

confidence: 99%

A Homing Peptide Modified Neutrophil Membrane Biomimetic Nanoparticles in Response to ROS/inflammatory Microenvironment for Precise Targeting Treatment of Ischemic Stroke

Dong,

Tang,

Zhang

et al. 2023

Adv Funct Materials

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Oxidative stress induced by ischemia‐reperfusion causes severe secondary injury in stroke patients. The blood‐brain barrier (BBB) and the challenges in targeting the stroke core hinder the therapeutic effect of drugs. This study introduces a precise biomimetic drug delivery system called SHp‐NM@Edv/RCD (SNM‐NPs), which possesses multiple stepwise targeting capabilities. SNM‐NPs are encapsulated by the neutrophil membranes (NMs) and exhibit a targeting effect (5.16‐fold) on the inflammatory microenvironment. The modification of stroke‐homing peptides (SHp) makes SNM‐NPs target damaged neurons faster, with a targeting efficiency 5.68 times higher than that of β‐cyclodextrins (RCD). Then, RCD encapsulated in SNM‐NPs responds to reactive oxygen species (ROS), leading to the release of edaravone (Edv), scavenges ROS, inhibits neuroinflammation, and reduces neuronal apoptosis by 90%. Mechanistically, SNM‐NPs deliver Edv precisely to the cerebral ischemia‐reperfusion injury (CIRI) site, resulting in the elimination of ROS, a decrease in the number of microglia, an improvement in tubulin expression in neurons, and the inhibition of neuronal apoptosis through Caspase 3 pathway. Preliminary experiments also show that SNM‐NPs exhibit a good safety profile both in intravenous therapy and in vitro cell experiments. As a result, SNM‐NPs hold promise for further development as effective and safe agents for target therapy of CIRI and other diseases.

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Section: Resultsmentioning

confidence: 99%

A Homing Peptide Modified Neutrophil Membrane Biomimetic Nanoparticles in Response to ROS/inflammatory Microenvironment for Precise Targeting Treatment of Ischemic Stroke

Dong,

Tang,

Zhang

et al. 2023

Adv Funct Materials

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“…At the end of 24 h reperfusion: neurological status of mice was assessed using the Zea Longa neurological scoring system: as mentioned earlier 30 . For this study: mice with scores ranging from 1 to 3 were included as the tMCAO model mice.…”

Section: Methodsmentioning

confidence: 99%

Neferine inhibits BMECs pyroptosis and maintains blood–brain barrier integrity in ischemic stroke by triggering a cascade reaction of PGC-1α

Zheng,

Zhu,

Qiu

et al. 2024

Sci Rep

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Blood–brain barrier disruption is a critical pathological event in the progression of ischemic stroke (IS). Most studies regarding the therapeutic potential of neferine (Nef) on IS have focused on neuroprotective effect. However, whether Nef attenuates BBB disruption during IS is unclear. We here used mice underwent transient middle cerebral artery occlusion (tMCAO) in vivo and bEnd.3 cells exposed to oxygen–glucose deprivation/reoxygenation (OGD/R) injury in vitro to simulate cerebral ischemia. We showed that Nef reduced neurobehavioral dysfunction and protected brain microvascular endothelial cells and BBB integrity. Molecular docking, short interfering (Si) RNA and plasmid transfection results showed us that PGC-1α was the most binding affinity of biological activity protein for Nef. And verification experiments were showed that Nef upregulated PGC-1α expression to reduce mitochondrial oxidative stress and promote TJ proteins expression, further improves the integrity of BBB in mice. Intriguingly, our study showed that neferine is a natural PGC-1α activator and illustrated the mechanism of specific binding site. Furthermore, we have demonstrated Nef reduced mitochondria oxidative damage and ameliorates endothelial inflammation by inhibiting pyroptosis to improve BBB permeability through triggering a cascade reaction of PGC-1α via regulation of PGC-1α/NLRP3/GSDMD signaling pathway to maintain the integrity of BBB in ischemia/reperfusion injury.

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“…There were 15 mice in each group. The mice in all groups, except the S group, underwent MCAO/R via wire insertion as described in our previous report (Shen et al, 2021). In brief, the mice were anesthetized with 1.5-2.0% iso urane, and their body temperature was maintained at 37.0 ± 0.5°C during the experiment.…”

Section: Animal Grouping and Interventionmentioning

confidence: 99%

Long noncoding RNA MALAT1 promotes angiogenesis through the caveolin-1/VEGF pathway after cerebral ischemic injury.

Lin

Pang

Shi

et al. 2023

Preprint

Self Cite

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Metastasis-associated lung adenocarcinoma transcript 1 (MALAT1), a long noncoding RNA (lncRNA), has been reported to potentially protect against cerebral ischemic injury. We investigated the role and underlying mechanism of MALAT1 in ischemic stroke. A mouse model of middle cerebral artery occlusion/reperfusion (MCAO/R) and a human brain microvascular endothelial cell (HBMEC) model of oxygen-glucose deprivation/reoxygenation (OGD/R) were established. The Zea Longa 5-point scale, VEGFR2/CD34 double immunofluorescence (IF), TUNEL staining, cell counting kit-8 (CCK-8) assay, tube formation assay, Transwell assay, and qRT–PCR were used to evaluate neurological deficits, endothelial cell (EC) proliferation, cell apoptosis, cell viability, in vitro angiogenesis, cell migration, and MALAT1 levels in mice, respectively. MALAT1 was found to promote cell migration and tube formation in vitro by affecting the caveolin-1/VEGF pathway. Downregulation of MALAT1 expression in vivo exacerbated cerebral ischemic injury as manifested by severe neurological deficits, elevation of apoptosis, and a decrease in the number of VEGFR2+/CD34+ endothelial progenitor cells (EPCs). These findings indicated that MALAT1 may promote angiogenesis after cerebral ischemic injury via the caveolin-1/VEGF pathway, thereby suggesting that MALAT1 is a therapeutic target for ischemic stroke.

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Treadmill exercise enhances synaptic plasticity in the ischemic penumbra of MCAO mice by inducing the expression of Camk2a via CYFIP1 upregulation

Cited by 16 publications

References 35 publications

A Homing Peptide Modified Neutrophil Membrane Biomimetic Nanoparticles in Response to ROS/inflammatory Microenvironment for Precise Targeting Treatment of Ischemic Stroke

A Homing Peptide Modified Neutrophil Membrane Biomimetic Nanoparticles in Response to ROS/inflammatory Microenvironment for Precise Targeting Treatment of Ischemic Stroke

Neferine inhibits BMECs pyroptosis and maintains blood–brain barrier integrity in ischemic stroke by triggering a cascade reaction of PGC-1α

Long noncoding RNA MALAT1 promotes angiogenesis through the caveolin-1/VEGF pathway after cerebral ischemic injury.

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