Objective To observe the difference between blood brain barrier and blood optic nerve barrier. Methods Twenty normal male SD rat sprime; optic nerve including prelaminar region, lamina cribrosa, retro-laminar region, intraorbital portion, intracanalicular portion, and intracranial portion respectively,and cerebral cortex were removed separately. Ultrastructure of endothelial cells was observed by electron microscopy. Immunohistochemical staining was used to detect the expression of transferrin receptor (OX-26) and metalloproteinase inducer (OX-47) and extravasation of fibrinogen around microvessels. Results The results of electron microscopy showed that endothelial cells of microvessels in each portion of optic nerves and cerebral cortex did share the same tight junctions. However, the number of plasmalemmal vesicles in prelaminar region was significantly more than that in cerebral cortex(P＜0.05);there was no significant difference between other parts of optic nerves (lamina cribrosa, retro- laminar region, intraorbital portion, intracanalicular portion, and intracranial portion)and cerebral cortex in the number of the plasmalemmal vesicles(Pgt;0.05). By immunohistochemical staining，the endothelial cells of microvessels in the prelaminar region showed no expression of the OX-26 and OX-47,but extravasation of fibrinogen around microvessels was found; b positive expression of OX-26 and OX-47 was observed in the endothelial cells of the microvessels in other parts of optic nerves (lamina cribrosa, retro-laminar region, intraorbital portion, intracanalicular portion, and intracranial portion) andcerebral cortex, and no fibrinogen was seen aro und the microvessels. Conclusions There is a significant difference between the endothelial cells of the microvessels in prelaminar region and cerebral cortex in the ultrastructure, markers expression, and permeability, so the microvessel s in prelaminar region lacks the typical blood brain barrier characteristics.The microvessels in other parts of optic nerves (lamina cribrosa, retro-laminar region, intraorbital portion, intracanalicular portion, and intracranial portion) have blood brain barrier properties due to its similar specialties as which in cerebral cortex. (Chin J Ocul Fundus Dis, 2006, 22: 390-393)
Ischemic stroke (IS) is one of the important diseases threatening human health. The occurrence and development of IS can trigger a series of complex pathophysiological changes, including damage to the blood-brain barrier, ion imbalance, oxidative stress, mitochondrial damage, which ultimately lead to the apoptosis and necrosis of nerve cells in the ischemic area. Impaired blood-brain barrier is a key factor for cerebral edema, hemorrhagic transformation and poor prognosis in patients with IS, and neuroinflammatory response plays an important role in the damage and repair of the blood-brain barrier. This article mainly focuses on the neuroinflammatory response mediated by glial cells, pro-inflammatory cytokines and matrix metalloproteinases and the related mechanisms of IS blood-brain barrier damage and repair, in order to provide new directions for the treatment of IS.
Febrile seizures (FS) are one of the most common neurological disorders in pediatrics, commonly seen in children from three months to five years of age. Most children with FS have a good prognosis, but some febrile convulsions progress to refractory epilepsy (RE). Epilepsy is a common chronic neurological disorder , and refractory epilepsy accounts for approximately one-third of epilepsies. The etiology of refractory epilepsy is currently complex and diverse, and its mechanisms are not fully understood. There are many pathophysiological changes that occur after febrile convulsions, such as inflammatory responses, changes in the blood-brain barrier, and oxidative stress, which can subsequently potentially lead to refractory epilepsy, and inflammation is always in tandem with all physiological changes as the main response. This article focuses on the pathogenesis of refractory epilepsy resulting from post-febrile convulsions.
It is a significant challenge to improve the blood-brain barrier (BBB) permeability of central nervous system (CNS) drugs in their development. Compared with traditional pharmacokinetic property tests, machine learning techniques have been proven to effectively and cost-effectively predict the BBB permeability of CNS drugs. In this study, we introduce a high-performance BBB permeability prediction model named balanced-stacking-learning based BBB permeability predictor(BSL-B3PP). Firstly, we screen out the feature set that has a strong influence on BBB permeability from the perspective of medicinal chemistry background and machine learning respectively, and summarize the BBB positive(BBB+) quantification intervals. Then, a combination of resampling algorithms and stacking learning(SL) algorithm is used for predicting the BBB permeability of CNS drugs. The BSL-B3PP model is constructed based on a large-scale BBB database (B3DB). Experimental validation shows an area under curve (AUC) of 97.8% and a Matthews correlation coefficient (MCC) of 85.5%. This model demonstrates promising BBB permeability prediction capability, particularly for drugs that cannot penetrate the BBB, which helps reduce CNS drug development costs and accelerate the CNS drug development process.
Neuromyelitis spectrum disease (NMOSD) is an immune-mediated inflammatory demyelinating disease of the central nervous system. The breakdown of the blood-brain barrier (BBB), as an important link in the pathogenesis of NMOSD, has an important impact on the occurrence, development and prognosis of the disease. It is generally believed that the aquaporin 4 antibody produced in the peripheral circulation crosses the BBB cause damage to the central nervous system, and there are components involved in the destruction of BBB in the occurrence and development of NMOSD disease. At present, little is known about the molecular mechanism of BBB destruction in NMOSD lesions and there is still a lack of systematic theory. Further research and exploration of the regulatory mechanism of BBB permeability and the manifestation of barrier destruction in NMOSD diseases are of great significance for understanding the pathogenesis of NMOSD, so as to achieve early diagnosis and discover new therapeutic and preventive targets.