Role of Protein Tyrosine Phosphatase 1B Inhibitor in Early Brain Injury of Subarachnoid Hemorrhage in Mice

Zhang, Zhonghua; Zhou, Xiaoming; Zhang, Xin

doi:10.3390/brainsci13050816

Cited by 2 publications

(1 citation statement)

References 47 publications

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“…Mouse experiments have shown that stress-induced glial cell boundaries can be formed on the first day after SAH, and pericytes regulate the formation of astrocyte glial boundaries through the EphA4/EphrinB2 signaling pathway, inhibiting inflammatory cell infiltration and improving neurological function [ 72 ]. Protein tyrosine phosphatase 1B inhibitor (PTP1B-in-1) can regulate the IRS-2/AKT signaling pathway, improve neuroinflammation and neuronal apoptosis, and exert neuroprotective functions [ 73 ]. In animal experiments, it was found that takinib alleviates EBI by targeting the inhibition of the TAK1-ROS-NLRP3 inflammasome signaling pathway [ 74 ].…”

Section: Potential Mechanisms Of Early Brain Injurymentioning

confidence: 99%

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature

Kang,

Tian,

Zhang

et al. 2024

Chin Neurosurg Jl

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Spontaneous subarachnoid hemorrhage (SAH), mainly caused by ruptured intracranial aneurysms, is a serious acute cerebrovascular disease. Early brain injury (EBI) is all brain injury occurring within 72 h after SAH, mainly including increased intracranial pressure, decreased cerebral blood flow, disruption of the blood-brain barrier, brain edema, oxidative stress, and neuroinflammation. It activates cell death pathways, leading to neuronal and glial cell death, and is significantly associated with poor prognosis. Ferroptosis is characterized by iron-dependent accumulation of lipid peroxides and is involved in the process of neuron and glial cell death in early brain injury. This paper reviews the research progress of ferroptosis in early brain injury after subarachnoid hemorrhage and provides new ideas for future research.

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Section: Potential Mechanisms Of Early Brain Injurymentioning

confidence: 99%

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature

Kang,

Tian,

Zhang

et al. 2024

Chin Neurosurg Jl

View full text Add to dashboard Cite

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Protein tyrosine phosphatase 1B contributes to neuropathic pain by aggravating NF‐κB and glial cells activation‐mediated neuroinflammation via promoting endoplasmic reticulum stress

Jiao,

Zhang,

Zhang

et al. 2024

CNS Neurosci Ther

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BackgroundNeuropathic pain is a prevalent and highly debilitating condition that impacts millions of individuals globally. Neuroinflammation is considered a key factor in the development of neuropathic pain. Accumulating evidence suggests that protein tyrosine phosphatase 1B (PTP1B) plays a crucial role in regulating neuroinflammation. Nevertheless, the specific involvement of PTP1B in neuropathic pain remains largely unknown. This study aims to examine the impact of PTP1B on neuropathic pain and unravel the underlying molecular mechanisms implicated.MethodsIn the current study, we evaluated the paw withdrawal threshold (PWT) of male rats following spared nerve injury (SNI) to assess the presence of neuropathic pain. To elucidate the underlying mechanisms, western blotting, immunofluorescence, and electron microscopy techniques were employed.ResultsOur results showed that SNI significantly elevated PTP1B levels, which was accompanied by an increase in the expression of endoplasmic reticulum (ER) stress markers (BIP, p‐PERK, p‐IRE1α, and ATF6) and phosphorylated NF‐κB in the spinal dorsal horn. SNI‐induced mechanical allodynia was impaired by the treatment of intrathecal injection of PTP1B siRNA or PTP1B‐IN‐1, a specific inhibitor of PTP1B. Moreover, the intrathecal administration of PTP1B‐IN‐1 effectively suppressed the expression of ER stress markers (BIP, p‐PERK/p‐eIF2α, p‐IRE1α, and ATF6), leading to the inhibition of NF‐κB, microglia, and astrocytes activation, as well as a decrease in pro‐inflammatory cytokines, including TNF‐α, IL‐6, and IL‐1β. However, these effects were reversed by intrathecal administration of tunicamycin (Tm, an inducer of ER stress). Additionally, intrathecal administration of Tm in healthy rats resulted in the development of mechanical allodynia and the activation of NF‐κB‐mediated neuroinflammatory signaling.ConclusionsThe upregulation of PTP1B induced by SNI facilitates the activation of NF‐κB and glial cells via ER stress in the spinal dorsal horn. This, in turn, leads to an increase in the production of pro‐inflammatory cytokines, thereby contributing to the development and maintenance of neuropathic pain. Therefore, targeting PTP1B could be a promising therapeutic strategy for the treatment of neuropathic pain.

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Role of Protein Tyrosine Phosphatase 1B Inhibitor in Early Brain Injury of Subarachnoid Hemorrhage in Mice

Cited by 2 publications

References 47 publications

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature

Ferroptosis in early brain injury after subarachnoid hemorrhage: review of literature

Protein tyrosine phosphatase 1B contributes to neuropathic pain by aggravating NF‐κB and glial cells activation‐mediated neuroinflammation via promoting endoplasmic reticulum stress

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