ABSTRACT
The disorder of autophagy lysosomal pathway (ALP) is an important pathogenesis of neuronal damage after cerebral ischemia, and the restoration of ALP may alleviate neuronal damage after cerebral ischemia. As the main transcription factor regulating ALP, transcription factor EB (TFEB) can directly regulate autophagosome generation, autophagosome-lysosome fusion, and autophagic flux by regulating the expression of autophagic genes and lysosomal genes. Therefore, regulating TFEB can alleviate ALP dysfunction and thereby reduce cerebral ischemic damage. This article reviews the structure, biological function of TFEB and its role in regulating ALP to alleviate neuronal damage after cerebral ischemia.
ABSTRACT
CCAAT/enhancer binding protein β (C/EBPβ), a transcriptional factor of the basic-leucine zipper family, can regulate the transcription activity of downstream target genes. After acute cerebral ischemia, the activity of C/EBPβ changes, and participates in the process of cerebral ischemia injury by regulating neuronal apoptosis and inflammation. This article reviews the molecular biological characteristics of C/EBPβ and its expression changes and role in acute cerebral ischemia, providing a basis for developing new neuroprotective drugs for acute cerebral ischemia using C/EBPβ as therapeutic target.
ABSTRACT
p75 neurotrophin receptor (p75 NTR) is a member of the tumor necrosis factor receptor superfamily, which interacts with tropomyosin receptor kinase (Trk) receptor or binds neurotrophic factors. It mediates a variety of complex signal transduction pathways, induces synaptic growth and affects cell survival. After acute cerebral ischemia, p75 NTR binds effector factors such as pro-nerve growth factor (proNGF) and sortilin, activating downstream apoptotic signal molecules and leading to neuronal death. Therefore, elucidating the pathways and molecular mechanisms of p75 NTR that mediate neuronal apoptosis in acute cerebral ischemia is of great significance for the development of new therapeutic drugs for acute cerebral ischemia.
ABSTRACT
ObjectiveTo investigate the expression change of cathepsin B (CathB) in the ventroposterior nucleus (VPN) of the ipsilateral thalamus after cortical infarction in rats.MethodsThe adult male Sprague-Dawley rats were randomly divided into either a sham operation group or a model group.The latter was further divided into postoperative 1-, 2-, 3-, 4-, and 8-week groups.A model of cerebral cortical infarction was induced by electrocoagulation the cortical branch of middle cerebral artery.Immunohistochemical staining and immunofluorescence were used to detect the protein expression and cellular localization of CathB in the VPN at each time point.ResultsThe expression level of VPN CathB in thalamus increased gradually after cerebral cortical infarction.It reached the peak at 4 weeks, and decreased at 8 weeks, however it was still higher than the control group (all P<0.05).The release of CathB from the lysosomes into the cytoplasm were found.In addition, the expression level of CathB in the activated astrocytes was significantly increased at 3 weeks after cerebral cortical infarction.ConclusionsDuring 1-8 week after cerebral cortex infarction, CathB in the VPN of the ipsilateral thalamus maintained higher expression level, suggesting that it might play a certain role in secondary degeneration in the thalamus after cerebral cortical infarction.