scholarly journals Ginseng Extracts, GS-KG9 and GS-E3D, Prevent Blood–Brain Barrier Disruption and Thereby Inhibit Apoptotic Cell Death of Hippocampal Neurons in Streptozotocin-Induced Diabetic Rats

Nutrients ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 2383
Author(s):  
Jee Youn Lee ◽  
Chan Sol Park ◽  
Hae Young Choi ◽  
Tae Young Yune
Keyword(s):  
Diabetes Mellitus ◽  
Cell Death ◽  
Blood Brain Barrier ◽  
Hippocampal Neurons ◽  
Apoptotic Cell ◽  
Diabetic Rats ◽  
Apoptotic Cell Death ◽  
Brain Barrier ◽  
Blood Brain

Type 1 diabetes mellitus is known to be linked to the impairment of blood–brain barrier (BBB) integrity following neuronal cell death. Here, we investigated whether GS-KG9 and GS-E3D, bioactive ginseng extracts from Korean ginseng (Panax ginseng Meyer), inhibit BBB disruption following neuronal death in the hippocampus in streptozotocin-induced diabetic rats showing type 1-like diabetes mellitus. GS-KG9 and GS-E3D (50, 150, or 300 mg/kg, twice a day for 4 weeks) administered orally showed antihyperglycemic activity in a dose-dependent manner and significantly attenuated the increase in BBB permeability and loss of tight junction proteins. GS-KG9 and GS-E3D also inhibited the expression and activation of matrix metalloproteinase-9 and the infiltration of macrophages into the brain parenchyma, especially into the hippocampal region. In addition, microglia and astrocyte activation in the hippocampus and the expression of proinflammatory mediators such as tnf-α, Il-1β, IL-6, cox-2, and inos were markedly alleviated in GS-KG9 and GS-E3D-treated group. Furthermore, apoptotic cell death of hippocampal neurons, especially in CA1 region, was significantly reduced in GS-KG9 and GS-E3D-treated groups as compared to vehicle control. These results suggest that GS-KG9 and GS-E3D effectively prevent apoptotic cell death of hippocampal neurons by inhibiting BBB disruption and may be a potential therapy for the treatment of diabetic patients.

scholarly journals Erratum: Lee et al. Ginseng Extracts, GS-KG9 and GS-E3D, Prevent Blood–Brain Barrier Disruption and Thereby Inhibit Apoptotic Cell Death of Hippocampal Neurons in Streptozotocin-Induced Diabetic Rats. Nutrients 2020, 12, 2383

Nutrients ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 1656
Author(s):  
Jee Youn Lee ◽  
Chan Sol Park ◽  
Hae Young Choi ◽  
Sung Hyun Chung ◽  
Mi Kyung Pyo ◽  
...  
Keyword(s):  
Cell Death ◽  
Blood Brain Barrier ◽  
Hippocampal Neurons ◽  
Apoptotic Cell ◽  
Diabetic Rats ◽  
Apoptotic Cell Death ◽  
Brain Barrier ◽  
Barrier Disruption ◽  
Blood Brain Barrier Disruption ◽  
Brain Barrier Disruption

The authors have requested that the following changes be made to their paper [...]

scholarly journals VX765 Attenuates Pyroptosis and HMGB1/TLR4/NF-κB Pathways to Improve Functional Outcomes in TBI Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-21 ◽  
Author(s):  
Zhezhe Sun ◽  
Mark Nyanzu ◽  
Su Yang ◽  
Xiaohong Zhu ◽  
Kankai Wang ◽  
...  
Keyword(s):  
Cell Death ◽  
Blood Brain Barrier ◽  
High Mobility ◽  
Brain Barrier ◽  
Neurological Deficits ◽  
Nf Kappa B ◽  
Neuroprotective Effects ◽  
Caspase 1 ◽  
Area Of Interest ◽  
Blood Brain

Background. Traumatic brain injury (TBI) refers to temporary or permanent damage to brain function caused by penetrating objects or blunt force trauma. TBI activates inflammasome-mediated pathways and other cell death pathways to remove inactive and damaged cells, however, they are also harmful to the central nervous system. The newly discovered cell death pattern termed pyroptosis has become an area of interest. It mainly relies on caspase-1-mediated pathways, leading to cell death. Methods. Our research focus is VX765, a known caspase-1 inhibitor which may offer neuroprotection after the process of TBI. We established a controlled cortical impact (CCI) mouse model and then controlled the degree of pyroptosis in TBI with VX765. The effects of caspase-1 inhibition on inflammatory response, pyroptosis, blood-brain barrier (BBB), apoptosis, and microglia activation, in addition to neurological deficits, were investigated. Results. We found that TBI led to NOD-like receptors (NLRs) as well as absent in melanoma 2 (AIM2) inflammasome-mediated pyroptosis in the damaged cerebral cortex. VX765 curbed the expressions of indispensable inflammatory subunits (caspase-1 as well as key downstream proinflammatory cytokines such as interleukin- (IL-) 1β and IL-18). It also inhibited gasdermin D (GSDMD) cleavage and apoptosis-associated spot-like protein (ASC) oligomerization in the injured cortex. In addition to the above, VX765 also inhibited the inflammatory activity of the high-mobility cassette -1/Toll-like receptor 4/nuclear factor-kappa B (HMGB1/TLR4/NF-kappa B) pathway. By inhibiting pyroptosis and inflammatory mediator expression, we demonstrated that VX765 can decrease blood-brain barrier (BBB) leakage, apoptosis, and microglia polarization to exhibit its neuroprotective effects. Conclusion. In conclusion, VX765 can counteract neurological damage after TBI by reducing pyroptosis and HMGB1/TLR4/NF-κB pathway activities. VX765 may have a good therapeutic effect on TBI.

scholarly journals The blood-brain barrier in primary CNS lymphomas: Ultrastructural evidence of endothelial cell death

1999 ◽  
Vol 1 (2) ◽  
pp. 89-100
Author(s):  
Peter P. Molnár ◽  
Brian P. O'Neill ◽  
Bernd W. Scheithauer ◽  
Dennis R. Groothuis
Keyword(s):  
Cell Death ◽  
Endothelial Cell ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Ultrastructural Evidence ◽  
Blood Brain ◽  
Endothelial Cell Death ◽  
Cns Lymphomas

Intracerebral Hemorrhage and Diabetes Mellitus: Blood-Brain Barrier Disruption, Pathophysiology, and Cognitive Impairments

2021 ◽  
Vol 20 ◽  
Author(s):  
Ghaith A. Bahadar ◽  
Zahoor A Shah
Keyword(s):  
Diabetes Mellitus ◽  
Intracerebral Hemorrhage ◽  
Blood Brain Barrier ◽  
Brain Barrier ◽  
Comorbid Condition ◽  
Barrier Disruption ◽  
Blood Brain Barrier Disruption ◽  
Blood Brain ◽  
Brain Barrier Disruption ◽  
The Impact

: There is a surge in diabetes incidence with an estimated 463 million individuals been diagnosed worldwide. Diabetes Mellitus (DM) is a major stroke-related comorbid condition that increases the susceptibility of disabling post-stroke outcomes. Although less common, intracerebral hemorrhage (ICH) is the most dramatic subtype of stroke that is associated with higher mortality, particularly in DM population. Previous studies have focused mainly on the impact of DM on ischemic stroke. Few studies have focused on impact of DM on ICH and discussed the blood-brain barrier disruption, brain edema, and hematoma formation. However, more recently, investigating the role of oxidative damage and reactive oxygen species (ROS) production in preclinical studies involving DM-ICH animal models has gained attention. But, little is known about the correlation between neuroinflammatory processes, glial cells activation, and peripheral immune cell invasion with DM-ICH injury. DM and ICH patients experience impaired abilities in multiple cognitive domains by relatively comparable mechanisms, which could get exacerbated in the setting of comorbidities. In this review, we discuss both the pathology of DM as a comorbid condition for ICH and the potential molecular therapeutic targets for the clinical management of the ICH and its recovery.

Intravenous Fibroblast Growth Factor Penetrates the Blood-Brain Barrier and Protects Hippocampal Neurons Against Ischemia-Reperfusion Injury

1998 ◽  
Vol 49 (1) ◽  
pp. 77-84 ◽  
Author(s):  
Pedro Cuevas M.D., Ph.D., F.A.C.A. ◽  
Fernando Carceller M.D., Ph.D. ◽  
Isabel Muñoz-Willery B.Sc., Ph.D. ◽  
Guillermo Giménez-Gallego B.Sc., Ph.D.
Keyword(s):  
Growth Factor ◽  
Reperfusion Injury ◽  
Fibroblast Growth Factor ◽  
Blood Brain Barrier ◽  
Hippocampal Neurons ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Brain Barrier ◽  
Fibroblast Growth ◽  
Blood Brain
Sign in / Sign up

Export Citation Format

Share Document