PTEN is a dual specificity phosphatase and is implicated in inflammation and apoptosis of cerebral ischemia and reperfusion (I/R) injury. Bisperoxovanadium (Bpv), a specific inhibitor of PTEN's phosphatase activity, has demonstrated powerful neuroprotective properties. We investigated the neuroprotective roles of Bpv in the rat model of middle cerebral artery occlusion (MCAO) cerebral I/R injury, and explored the modulation of inflammatory mediators and PI3K/Akt/GSK-3β pathways by Bpv. Our results showed that treatment with Bpv (0.2 mg/kg/day) significantly decreased neurological deficit scores at 7 days after MCAO and infarct volume at 4 days after MCAO. The IL-10 concentration was increased and TNF-α concentration was decreased in the ischemic boundary zone of the cerebral cortex at 4 days after MCAO by Bpv. Furthermore, Bpv (0.2 mg/kg/day) treatment significantly reduced PTEN mRNA and protein levels and increased PI3K, Akt and p-GSK-3β proteins expression in the ischemic boundary zone of the cerebral cortex at 4 days after MCAO. In conclusions, Bpv treatment demonstrates neuroprotective effects on cerebral ischemia and reperfusion injury of ischemic stroke rats and is associated with its modulation of inflammatory mediator production and up-regulation of PTEN downstream proteins PI3K, Akt and p-GSK-3β.
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http://dx.doi.org/10.1016/j.neulet.2015.06.040 | DOI Listing |
Chin J Integr Med
January 2025
Department of Ultrasound in Medicine, the Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, 310009, China.
Objective: To evaluate the therapeutic effects of Kuanxiong Aerosol (KXA) on ischemic stroke with reperfusion and elucidate the underlying pharmacological mechanisms.
Methods: In vivo pharmacological effects on ischemic stroke with reperfusion was evaluated using the transient middle cerebral artery occlusion (t-MCAO) mice model. To evaluate short-term outcome, 30 mice were randomly divided into vehicle group (n=15) and KXA group (n=15).
Chin Med
January 2025
Yunnan Key Laboratory of Integrated Traditional Chinese and Western Medicine for Chronic Disease in Prevention and Treatment, Key Laboratory of Acupuncture and Massage for Treatment of Encephalopathy, College of Acupuncture, Tuina and Rehabilitation, Yunnan University of Traditional Chinese Medicine, Kunming, China.
Objective: Electroacupuncture has been shown to play a neuroprotective role following ischemic stroke, but the underlying mechanism remains poorly understood. Ferroptosis has been shown to play a key role in the injury process. In the present study, we wanted to explore whether electroacupuncture could inhibit ferroptosis by promoting nuclear factor erythroid-2-related factor 2 (Nrf2) nuclear translocation.
View Article and Find Full Text PDFTransl Stroke Res
January 2025
Department of Neurology, McGovern Medical School, The University of Texas Health Science Center at Houston, 6431 Fannin Street, Houston, TX, 77030, USA.
The role of chromatin biology and epigenetics in disease progression is gaining increasing recognition. Genes that escape X chromosome inactivation (XCI) can impact neuroinflammation through epigenetic mechanisms. Our previous study has suggested that the X escapee genes Kdm6a and Kdm5c are involved in microglial activation after stroke in aged mice.
View Article and Find Full Text PDFFront Physiol
December 2024
Department of Medical Physics and Medical Informatics, University of Szeged, Szeged, Hungary.
Introduction: Cerebral ischemia leads to multiple organ dysfunctions, with the lungs among the most severely affected. Although adverse pulmonary consequences contribute significantly to reduced life expectancy after stroke, the impact of global or focal cerebral ischemia on respiratory mechanical parameters remains poorly understood.
Methods: Rats were randomly assigned to undergo surgery to induce permanent global cerebral ischemia (2VO) or focal cerebral ischemia (MCAO), or to receive a sham operation (SHAM).
Exp Neurol
December 2024
Department of Neurology, Henry Ford Health System, Detroit, MI 48202, United States of America. Electronic address:
Dendritic and axonal plasticity, which mediates neurobiological recovery after a stroke, critically depends on the mitochondrial function of neurons. To investigate, in vivo, neuronal mitochondrial function at the stroke recovery stage, we employed Mito-tag mice combined with cerebral cortical infection of AAV9 produced from plasmids carrying Cre-recombinase controlled by two neuronal promoters, synapsin-I (SYN1) and calmodulin-kinase IIa to induce expression of a hemagglutinin (HA)-tagged enhanced green fluorescence protein (EGFP) that localizes to mitochondrial outer membranes of SYN1 positive (SYN) and CaMKIIa positive (CaMKIIa) neurons. These mice were then subjected to permanent middle cerebral artery occlusion (MCAO) and sacrificed 14 days post stroke.
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